14.4- ACLS-2013-e-PUB-AFlutter-Cosio PDF-(12-26.21-2014)-LOCK pdf
14.4- ACLS-2013-e-PUB-AFlutter-Cosio PDF-(12-26.21-2014)-LOCK pdf
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  2. Section 00.1-Table of CONTENTS -14.0 –SVT: PRACTICE TRACINGS14.4.0 –SVT Practice Example-414.4.1 –SVT: What is the Rhythm?14.4.2 –What is the Rhythm in Figure 14.4.1-1?14.4.3 –KEY Points: ECG Diagnosis of AFlutter14.4.4 –AFlutter: Diagnostic Use of a Vagal Maneuver14.4.5 –KEY Clinical Points: Regarding AFlutter14.4.6 –AFlutter: Appearance on a 12-Lead Tracing14.4.7 –AFlutter: Variable Conduction14.4.8 –AFlutter: Unusual 3:1 AV Conduction14.4.9 –AFlutter: Is it AFlutter or Atrial Tach with Block?14.4.10 –AFlutter: Is it AFib? –AFlutter –or Fib-Flutter?14.4.11 –AFlutter: Real or Artifact?14.4.12 –Beyond-the-Core: Typical and Atypical AFlutter14.4.13 –AFlutter: Treatment Priorities14.4.14 –Summary: Treatment of New-Onset AFlutter
  3. Section 14.4.0 –SVTPractice Example-4 (AFlutter)14.4.1 –SVT: What is the Rhythm?The patient is a hemodynamicallystable adult who presents to the ED with the rhythm below. The QRSis confirmedto be narrowon 12-lead ECG. •Whatis the Rhythm?•Clinically–What should you do next?Figure 14.4.1-1: The patient is stable. What is the rhythm? What next?14.4.2 –What is the Rhythmin Figure 14.4.1-1?The rhythm in Figure 14.4.1-1is rapid and regular. We are told that a 12-leadECGconfirmsQRS narrowingin allleads. The rate is close to150/minute. Normal atrial activity is notseen (the small, rounded upright deflection preceding each QRS has a PR interval that appears too short for normal conduction). We have therefore described a regularSVT at~150/minutewithoutsign of normal atrial activity. This description should again bring to mind LIST #2of the 3 entitiesto considerin the differential diagnosis of a regularSVT(Table 14.4.2-1):•Although normalatrial activity is notpresent in Figure 14.4.1-1 –it is likely that someform of atrial activity ispresent (be this the upright rounded deflection preceding each QRS with short PR–or–the negative deflection midway between each QRS).Table14.4.2-1: Common causes of a regularSVT rhythm when sinus P waves are not clearly evident. (NOTE: We previously presented this Table in Sections13.6and 14.3.2).Regarding the differentialdiagnosisfor a regularSVT rhythmwithout normal sinus P waves (such as that seen in Figure 14.4.1-1) –We can state the following:•Overall regularityof the rhythm rules outAFib/MAT.
  4. •The 3 most commoncausesof a regularSVTto consider are: i)Sinus tachycardia; ii)Atrial flutter; andiii)PSVT.The rateof ~150/minutethat is seen in Figure 14.4.1-1 could be consistent with anyof these 3 diagnoses. That said –a rate of ~150/minute for a regularSVT of uncertainetiology should suggestAFlutteras our first consideration(See Section 14.4.3).•Obtaining a 12-lead ECGand/oruse of a vagalmaneuvermay be helpful for confirming the diagnosis. 14.4.3 –KEY Points: ECG Diagnosis of AFlutterDefinitive diagnosisof the rhythm in Figure 14.4.1-1issimplynotpossible from the single-leadtracing we are given. That said —We stronglysuspect AtrialFlutteras the diagnosis:•In our experience —AFlutteris by far the most commonly overlookedrhythm diagnosis. It is easyto overlook —because flutter waves are notalways evident in all leads. AlwayssuspectAFlutter (until proven otherwise) —whenever there is a regularSVTat ~150/minutewithoutnormal atrial activity.This is precisely what we see in Figure 14.4.1-1.•The diagnosisin this casecan be confirmed with a vagalmaneuver (Section 14.4.4).•NOTE:Initiation of treatmentfor SVT rhythmsin the hemodynamically stablepatient need notnecessarily await definitive diagnosis.Depending on the clinical situation –one may (or may not) hold off on starting treatment until “the answer” is known.14.4.4 –AFlutter: Diagnostic Use of a Vagal ManeuverFigure 14.4.4-1shows the effect of CSM (Carotid Sinus Massage)on the rhythm presented at the beginning of this Section (Figure 14.4.1-1).•Whathappens with carotid massage?Figure 14.4.4-1: What happens afterCSM (large red arrow)is applied?(See text).ANSWER to Figure 14.4.4-1:Application of CSM slowsthe ventricular responseof the regular SVT rhythm in Figure 14.4.1-1. This facilitatesrecognition of regular sawtoothatrial activityat ~300/minute(regular small red arrows occurring each large box = 300/minute). •Application of a vagal maneuver (CSM)in Figure 14.4.4-1 confirmsthe diagnosisofAFlutter (the onlyrhythm that producesregular atrial activity at ~300/minute is AFlutter).•Following carotid massage –we count 4 negativedeflections within each R-R interval. Thus –CSM has reducedthe rate of AV conduction in this example of AFlutter from 2:1 to 4:1.
  5. 14.4.5 –KEY ClinicalPoints: Regarding AFlutterAtrial flutter ischaracterized by a special pattern of regularatrial activity that in adults almostalways (and almost magically) occurs at a rate of ~300/minute (250-to-350/minute = usual range). AFlutter typically manifests a sawtoothappearance that is usually best seen in the inferiorleads (and in lead V1). At times, flutter waves may be verysubtle —and only seen in a handful of leads. •The mostcommonventricular response to AFlutter (by far!) —is with 2:1 AV conduction. As a result, the ventricular rate with untreatedAFlutterwill usually be closeto 150/minute (300/2=150/minute). NOTE:The atrial rate may be lessthan 250-300/minute —IFthe patient is already takingcertain antiarrhythmic drugs.•The next most common ventricular response to AFlutter is 4:1 AV conduction (atrial rate ~300/minute; ventricular rate ~75/minute).•Occasionally —AFlutter may manifest a variable(irregular) ventricular response. In such cases —there will be an irregularly irregularventricular response resembling AFib (except for the presence of regularly occurring sawtooth flutter waves).•Oddconduction ratios (1:1; 3:1; 5:1) are uncommonfor AFlutter (with the exception being the patient with WPW who is prone to 1:1 AV conduction).SemanticPoint:—It is best notto say the example of AFlutter in Figure 14.4.1-1represents “2:1 AV block”. The term “block” implies pathology. Rather than being a bad thing that only 1 out of every 2 flutter impulses arriving at the AV node is conducted —it is indeed very fortunate that an intrinsic AV nodal refractory period exists that normally prevents1:1 AV conduction from occurring. Thus, 2:1 AV conductionwith AFlutteris “physiologic”(it is beneficial because it prevents an excessively fast ventricular rate).14.4.6 –AFlutter: Appearance on a 12-Lead TracingIt is helpful to become comfortable with several aspects regarding the recognition of AFlutter on 12-lead ECG (Figure 14.4.6-1).Figure 14.4.6-1: Atrial flutter on 12-lead ECG(See text).
  6. Note in Figure 14.4.6-1that the rhythm is a regularSVT (narrow-complex tachycardia) at a rate of ~150/minute. AFlutter should be assumed until proven otherwise (Section 14.4.3).•Typically with AFlutter –flutter waves will be best seen in the 3 inferior leads (II,III,aVF). This is the case in Figure 14.4.6-1.•We KNOW the rhythm in figure 14.4.6-1 is notsinus. This is because there is noupright P wave with fixed PR interval preceding the QRS in lead II. Instead –there is a negative deflection preceding each QRS in lead II (ifnot 2 negative deflections within each R-R interval in this lead). •Always look for a longlead II rhythm stripwhen contemplating the diagnosis of AFlutter. This is seen at the bottom of the tracing in Figure 14.4.6-1. Regularly occurring redarrowsmarkout negative atrialactivityat an approximate rate = 300/minute. The only arrhythmia that produces regular atrial activity at ~300/minute is AFlutter.•Use of caliperstremendously facilitates the diagnostic process. There is no easier way to identify ifbaseline deflections are regularly occurring or not.•Flutter waves are notalways seen in all leads on a 12-lead tracing. This is why we always meticulouslysearch each of the 12 leads for clues to underlying atrial activity. In Figure 14.4.6-1 –bluearrowshighlight flutter waves in several additional leads where they are seen. Note that flutter waves will often manifest positivedeflections in leads aVR and V1 (as they do here). There is no indication of AFlutter in leads I or V2 of this tracing.•Assessment of ST-T wave morphology is made more difficult when the underlying rhythm is AFlutter. This is because sawtoothflutter activity may maskunderlying ST-T wave changes.•Beyond-the-Core:There is actually slight irregularity in the early part of the rhythm in Figure 14.4.6-1 (See beat X). Despite slightly earlier-than-expectedoccurrence of this QRS complex –note how regular flutter activity (red arrows) nevertheless continues in the long lead II rhythm strip.Whether beat X represents fusion from a PVC or aberrant conduction from transient change in AV conduction ratio to 3:2 Wenckebach within the AV node is unimportant.What counts is persistence of underlying flutter activity that proves AFlutter as the diagnosis.14.4.7 –AFlutter: Variable ConductionAlthough AFlutter most often manifests either 2:1 or 4:1 AV conduction –it may also commonly present with a variableventricular response. When this happens –the ventricular response will resemble that of AFib in being irregularlyirregular (Figure 14.4.7-1).•The diagnosis of AFlutter is made by recognition of regular sawtoothatrial activity at a rate closeto 300/minute.Figure 14.4.7-1: AFlutter with variable ventricular response. The ventricular response is irregularlyirregular and resembles AFib –but regular sawtoothatrial activityat a rate closeto 300/minute identifies the rhythm as AFlutter.
  7. 14.4.8 –AFlutter: Unusual 3:1 AV ConductionOdd conduction ratios are distinctly uncommon for AFlutter. Most non-cardiologist providers only rarely encounter AFlutter with 1:1 or 3:1 AV conduction. Higher level odd ratios areevenrarer.•Figure 14.4.8-1showsan example of AFlutter with 3:1 AV conduction. The ventricular response in this tracing is regular at a rate of ~85/minute. There are 3 flutter waves for each QRS (therefore an atrial rate of 85 X 3=255/minute).•There will usually be “something else” going onmedically with the patient whenyou encounter AFlutter with an oddconduction ratio. Many such patients will be receiving one or moreantiarrhythmic drugs (that may slow the flutter rateand affect AV conduction ratio). AFlutter with 1:1 AV conduction (ventricular rate close to 300/minute) –should lead one to inquire IFthe tracing is from a child who may havecongenital heart disease and/ora patientof any agewith WPW(Section 12.9). BOTTOM Line:You will probably only rarelysee AFlutter with an odd conduction ratio, if at all ...•Beyond-the-Core:As opposed to the situation forAFlutter with variable ventricular response (Figure 14.4.7-1) –in which the distancebetween the flutter wave immediately preceding each QRS and the QRScomplex itself varies–there isa constant flutter-to-QRSdistancebefore each QRS complexin Figure 14.4.8-1. This confirms that there isconduction of one out of every 3 flutter waves in this tracing!Interestingly –it is notthe flutter wave closest to the QRS that conducts. Instead,bombardment of the AV node by 255flutter waveseach minute results in relative refractorinessof the AV node to forward conduction (ie, it is likely that the flutter wave that conducts eachthird impulse to the ventricles is either #1 or #2 –but not #3 in Figure 14.4.8-1).Figure 14.4.8-1: Atrial flutter with 3:1 AV conduction. Odd AV conduction ratios for AFlutter (such as 1:1 or 3:1) are distinctly uncommon(See text).14.4.9 –AFlutter: Is it AFlutter or Atrial Tach with Block?In the dayswhen Digoxin was regularly used for treatment of heart failure and atrial fibrillation –atrialtachycardia withblock(previously known as PAT = Paroxysmal Atrial Tachycardia with block) was commonly seen as a manifestation of digoxintoxicity.So characteristic was atrial tachycardia with block of Digoxin toxicity –that patients taking Digoxin were presumedto be toxic IFthis arrhythmia was seen regardlessof what the serum digoxin level was.•Given that AFlutter is one of the few arrhythmias notattributable to digoxin toxicity –much attention used to be focused on distinguishing between atrial tachycardia with block vs AFlutter.Ifthe arrhythmia was deemed “PAT with block” –then Digoxin was withheldfor presumed toxicity. If on the other hand, the rhythm was felt to represent AFlutter with 2:1 AV conduction –then additionalDigoxin was often recommended in hope of slowing down the ventricular response.
  8. While the above describedapproach to management has long ago been rendered obsolete by numerous advancements in treatment of supraventricular tachyarrhythmias (as well greatly reduced use of Digoxin, such that digoxin toxicity is seen far less often than it used to be) –it is nevertheless insightful to draw upon this historical perspective in interpreting the rhythm shown in Figure 14.4.9-1.•Is the rhythm in Figure 14.4.9-1likely to represent AFlutter oratrial tachycardia with block?•Clinically –Does it matter?Figure 14.4.9-1: Is the rhythm shown likely to represent AFlutter or atrial tachycardia with block? How can you tell? Clinically –Does it matter?(See text).ANSWER to Figure 14.4.9-1:The tracingin right-sidedmonitoring lead MCL-1 shows a regularSVT rhythm at a ventricular rate of ~115/minute.Two P waves are seento occurwithin each R-R interval. The P-P interval is regular at a rate of ~230/minute (ie, 115 X 2 = 230/minute).•In favor of AFlutteras the etiology of rhythm in Figure 14.4.9-1 –is regular and rapid atrial activity with a peaked upward deflection in right-sidedlead MCL-1. That said –the atrial rate of 230/minute is belowthe usual atrialrate range for untreatedAFlutter (of 250-350/minute) –andthe expected “sawtooth” pattern of AFlutter is missingin this lead.•We are nottold if this patient is taking an antiarrhythmicagent(such as flecainide, amiodarone, sotalol, etc.) that might slow the atrial rate of flutter. We are also nottold if the patient is taking Digoxin (less likely in 2013 than in the past –though still a possibility to inquire about).•In favor of ATach (Atrial Tachycardia)with2:1 AV Block–is the atrial rate of 230/minute (which isbelow the usual range for untreated AFlutter –butwithin theupper raterange for atrial tachycardia) –and the isoelectricbaseline (rather than sawtooth) in this lead.BOTTOM Line:It is impossibleto be sure of the rhythm diagnosissolely from the rhythm strip seen in Figure 14.4.9-1 withoutthe benefit of additional information. Neitherrate norbaseline appearance (sawtooth vs isoelectric baseline) have been shown to reliably distinguish between ATach vs AFlutter.•Obtaining a 12-lead ECGmay be helpful (it might reveal a typical sawtooth pattern in other leads).•Knowing IF this patient was on some rate-slowingantiarrhythmic agent (which would favor AFlutter) and/or was taking Digoxin (which would increaseconcern about digoxin toxicity) is critically important.•Beyond-the-Core:Assuming this patient is not on Digoxin –the terminology used to describe thearrhythmiaseen in Figure 14.4.9-1isfarless important than the overall clinical conceptsinvolved.As will be discussed in Section 14.4.12 –What used to be classified as “atrial tachycardia”in non-digoxin toxic patients is now often referred to as an “atypical”formof AFlutter.
  9. Included within the broad category of “atypical” AFlutter rhythms are various types of atrial tachycardias that may arise from anywhere within the atria or neighboring pulmonary veins. Some atrial tachycardias may be “focal” or automatic (often recognizable by non-sinus P wave appearance–“warm up” phenomenon until the ectopic tachycardia is established –relatively slower rate –and on occasion slightly variable P-P intervals). But other atrial tachycardias may be much faster, perfectly regular, lack an isoelectric baseline –andbe clinically indistinguishablefrom AFlutter based on ECG appearance.•Clinical “Take-Home”Point:While we admittedly cannot be certain whether the arrhythmia in Figure 14.4.9-1 represents ATach or AFlutter –initialtreatment considerationswill be the sameonce Dig toxicity has been ruled out (SeeSection 14.4.13). From a non-specialist perspective –longterm management will also be similar (ie, EP referral if the arrhythmia is persistent or recurs).14.4.10–AFlutter: Is it AFib? –AFlutter–or “Fib-Flutter”?The rhythm shown in Figure 14.4.10-1 often defies classification. The initial portion of this tracing resembles the sawtooth pattern of AFlutter. On the other hand,erratic undulations in the baseline during the latter portionof this rhythm stripare clearly more suggestive of the coarse fib wavesof atrial fibrillation.As a“compromise” –the term “AFib-Flutter”has been proposed.•Despite anatomic imperfection (the rhythm is generally eitherAFib or AFlutter) –descriptive use of the term “AFib-Flutter” accurately conveys the ECG picture of atrial activity intermediatebetween AFib and AFlutter. •Strictly speaking –the initial portion of this rhythm strip doesnot qualify as “atrial flutter” because atrial activity is toofast (over 350/minute in parts); irregular; and notconsistent in atrial morphology. That said –We would accept as “correct” aninterpretation of the rhythm in Figure 14.4.10-1aseitherAFib (here with a very slow ventricular response) –or–“AFib-Flutter”. The point to emphasize is that in the absenceof consistent regular flutter activity throughoutthe rhythm strip–arhythmsuch as that seen in Figure 14.4.10-1behaves clinicallyas if it wasAFib.Figure 14.4.10-1: AFib with veryslow ventricular response. Alternatively –one might classify this rhythm as “AFib-Flutter”. Thisrhythm behavesclinicallyas AFib(See text).14.4.11–AFlutter: Real or Artifact?The rhythm in Figure 14.4.11-1 was interpreted as atrial flutter.•Do youagreethat the rhythm in Figure 14.4.11-1 is AFlutter?Figure 14.4.11-1: Is this AFlutter?(See text).
  10. ANSWER to Figure 14.4.11-1:We concludethis group ofillustrative tracings with an example of what atrial flutteris not. The rhythm in Figure 14.4.11-1 is notAFlutter. Instead –there is underlying sinusrhythm. The numerous small undulations that populatethe baseline represent artifact. Reasons why we knowthisrhythmis notAFlutter include the following:•Distinct sinus P waves are seen preceding each QRS complex with fixed and normal PR interval (red arrows in Figure 14.4.11-2).•These normal sinus P waves are unaffectedby the continuous, smaller-amplitudeand irregularbaseline undulations. In fact –sinus P waves are superimposedon this baseline artifact.•We looked at the patient. Turns out that the patient had restingtremor.Figure 14.4.11-2: Arrows have been added to Figure 14.4.11-1 illustrating thatsinus P waves are superimposedonthesmaller amplitude baseline artifactundulations(See text).BOTTOM Line:It is easyto be fooled by artifact. The best wayto prevent this from happening is to develop healthy respect for the gamut of “real appearing”arrhythmias that artifact distortion may produce.•Looking at the patientmay provide invaluable insight. Tapping, scratching, coughing, shaking, shivering, seizing and tremor are but a few of the common causes of artifactualarrhythmias.•The frequency of a resting Parkinsoniantremoris often quite close to the frequency of flutter waves. In addition to observation of the patient –clues that Parkinsonian tremor is the cause of an arrhythmia mimic (such as that seen in Figure 14.4.11-2) are irregularity ofrate anddeflection morphology (whereas both are consistent with atrial flutter).14.4.12–Beyond-the-Core: Typical and Atypical AFlutterThere is more than a single type of “atrial flutter”. With typicalAFlutter(which makes up over 80% of cases) –the sawtoothpattern of flutter is extremely well visualized in the inferiorleads and in lead V1. The flutter wavefront almost always manifests CCW (counterclockwise) rotation around the tricuspid ring(ergo alternate designation as CTI-dependent = Cavo-Tricuspid-Isthmus-dependent flutter). In ~10% of cases–typicalAFlutter will follow the same path through the atria, but for unexplained reasons with CW (clockwise) instead of CCW rotation around the tricuspid ring (ie, “reverse” typical flutter). In these patients with “reverse” typical flutter –the same leads reveal the diagnosis, but instead of upright flutter waves in V1 there maybe a double negative (W-shaped) flutter wave in V1. •The appearance of flutter waves on the surface ECG depends on many factors including pathway through the atria, rotation direction of the impulse (CCW or CW), presence of scarringfrom prior infarction, cardiomyopathy, previous procedure, etc. Realize that even with “typical” (CTI-dependent)
  11. AFlutter–flutter waves maybe primarily positive, negative or biphasic in inferior leads and V1 (which are the leads where flutter wavesare usually seenbest).•While NOT important for non-electrophysiologists to distinguish between the differing ECG appearenceofthe various types ofAFlutter –it IS clinically relevantto be aware that atypicalAFlutter formsmay be seen in 10-20% of cases, in which the path through the atria is different andAFlutter may be present despite absenceof a prominent “sawtooth” pattern. As a result –atypicalAFlutter may be more difficult to recognize on ECG.•NOTE:What used to be classified as “atrial tachycardia”in non-digoxin toxic patients –is now often referred to asa form of“atypical”AFlutter.While some atrial tachycardias may be relativelyeasy to distinguish from AFlutter (isoelectric baseline, variation in P-P interval, ectopic “warm-up” or “cool-down” period before or after tachycardia) –this is not always the case. Instead –rapid atrial tachycardia in a scarred atrium may sometimes closelymimicAFlutter, such that neitherisoelectric baseline norrate overor under240/minute serve as distinguishing features.•BOTTOM Line:Long-term management of the typical and atypical AFlutter(including atrial tachycardias) belongsin the realm of the EP cardiologist. Fortunately –distinction between the various formsof these arrhythmiasis notessential by the nonspecialist –andinitialtreatment considerations are essentially the same (Section 14.4.13). 14.4.13–AFlutter:Treatment PrioritiesBy way of clinical perspective –AFlutter isfar lesscommon in its clinical occurrence than AFib. That said —there are many similarities in the approach to these 2 arrhythmias, such that it is useful to compare clinical aspects of each (realizing that distinction between the two is not always clear –and some patients may go back-and-forth from AFib to AFlutter).We note the following general concepts:•The samedrugsare used to slowthe ventricularresponseto bothAFib andAFlutter (ie, Diltiazem/Verapamil; Beta-blockers; Digoxin). That said —it will often be moredifficult to control the ventricular rate of AFlutter with the use of drugs.•The samedrugsare also used for AFib andAFlutter when attempting medicalconversion—and/or for maintenanceof sinus rhythm (ie, Amiodarone; Sotalol; Propafenone; Flecainaide). An AV nodal rate-controllingagent(Diltiazem/Verapamil; Beta-blocker)willoften be used at the same time with patients in AFlutter in hope of avoiding the phenomenon of 1:1 AV conduction that might otherwise arise from slowing the atrial rate of flutter.•Ibutilide (1 mg IV over 10 minutes; may repeat once) —works better for converting AFlutter (~60-70% success) vsonly ~30-40% success with this drug for converting AFib.•SynchronizedCardioversion —is more effective for converting AFlutter (it almost always works!) –compared to a lowersuccess rate for acute cardioversion of AFib. Lowerenergies (~50 joules) usually work for the more organized atrial rhythm of flutter (vs higher energies that are oftenneeded to cardiovert AFib).
  12. •LongtermAnticoagulation —isrecommended for AFlutter (although the risk of thromboembolism appears to be less than it is for AFib).•Persistent AFlutter is more easily treated (and more often cured) with catheterablation. Awareness of this fact should lowerone’s threshold for referralto an EP(ElectroPhysiology) cardiologistin the event AFlutter recurs following successful cardioversion.Realizing that it will often be much moredifficult to slow the ventricular rate of a patient in AFlutter –initial rate-slowing is most commonly attempted with IV Diltiazem(bolus and infusion—Section 13.15):•DILTIAZEM—Give ~15-20 mg IV bolus. IF no response —May follow in 15 minutes with a 2nd bolus (of ~25mgIV). •May then start IV infusionat 10 mg/hourto maintainrate control (usual range ~5-15mg/hour range).•Alternatively —an IV Beta-blockercould be used insteadof IV Diltiazem (Section 13.16) —especially if increased sympathetictone is a likely contributingcause of AFlutter.•Be sure to replaceMg++andK+ (depletion of one or both of these electrolytes may exacerbate the arrhythmia).•Digoxin —is much lesscommonly used in 2013 for treatment of AFlutter than in the past (though it may help on occasion as a supplemental agent for AFlutter with acute heart failure).•Synchronizedcardioversionoffers a high rate of success in the acute situation. Whether or not to proceed with this intervention in the acutesetting either initially orif medical treatment fails to adequately control the ventricular response is a decision to be made by the emergency care provider at the bedside.14.4.14 –Summary:Treatment of New-Onset AFlutterInitial priorities and clinical approach to new-onsetAFlutterarein general quitesimilar to those for AFib: •Before all else —Ensure the patient with newAFlutter is hemodynamicallystable (they almost always will be).•Look for a potentially correctableunderlying causeof AFlutter (ie, improving oxygenation in a COPD patient may facilitate spontaneous resolution of AFlutter).•Consider early on the need for anticoagulation.•Optimize fluid balance and electrolyte (K+/Mg++) status.•Slowthe ventricularresponseIFit is rapid (as it most often will be with new-onset AFlutter). IV Diltiazem (bolus and drip) —is most commonly used (although as for AFib —a Beta-blocker may be used instead).•Realize that AV nodal blocking drugs will notalways succeed in slowing the ventricular response. IFAFlutter persists despite initial treatment measures (especiallywhen the ventricular response to AFlutter remains fast) —referral may be in order. This is because medical conversion (with drugs such as Amiodarone –Sotalol –Flecainide –Propafenone –Ibutilide) —and/ornonemergent synchronized cardioversion entail aspects of treatment beyond the scope of the usual noncardiologist emergency care provider.
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