That ends the cycle, as there will be no ventricular action potential to reenter and stimulate the atria, which means that the next pulse should be a good honest sinus beat. AV nodal blocking agent ie, adenosine, verapamil, beta blockers should be instituted. We suggest intravenous adenosine rather than intravenous verapamil as the initial choice based on its efficacy and short half-life.
In antidromic SVT, the action potential conducts to the ventricle initially via the accessory pathway, then wanders shambolically around the ventricles producing a weird wide QRS, and then propagates up the AV node in an unnatural retrograde manner. It then goes straight back down into the ventricle via the accessory pathway, and the whole thing repeats cyclically.
So, consider what might happen if the AV node were blocked. The ventricle is now only depolarised by the accessory pathway, so the QRS will be weird and wide, but now that the AV node is blocked, theoretically the block should have the exact same effect as in orthodromic SVT, i.
If the diagnosis is not certain, the patient should be considered to have an undiagnosed wide QRS tachycardia ". Interpreting this literally, it would appear that they would also recommend AV blockers for antidromic SVT, just as they would for orthodromic SVT, just as long as you are absolutely sure that it is antidromic. Or orthodromic.
Atrial fibrillation in WPW is a hideous thing. The erratic atrial action potentials getting propagated down the accessory pathway are a source of bizarre broad QRS complexes which bounce crazily around the ventricle and create an electrical environment richly conducive to early afterdepolarisations. These are hopefully balanced by some normal narrow-complex action potentials propagating down the AV node, which should depolarise the ventricle in a more organised fashion, hopefully preventing any ventriculofibrillatory shenanigans by putting enough of the ventricle into an absolute refractory period.
Now, consider using an AV blocker in this scenario. The AV node no longer conducts any normal potentials, and ventricular activity is being driven solely by the total chaos of the fibrillating atria. The ventricular rate is no longer limited by the stabilising apperance of "properly" conducted beats, and the ventricle ends up stimulated by a cacophony of action potentials arriving at some rate between per minute.
The effect is illustrated by the image below, which was shamelessly stolen from Shah via this excellent blog:. Note that adenosine is not required for this. The model answer to Question 3. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since , public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity.
It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway. The table below has been compiled with the use of the belowlisted references and the UpToDate article on this topic.
Springer Netherlands, Gulamhusein, S. Munger, T. Narula, Onkar S. Scheinman, Melvin M. Keating, L. Morris, and W. Wolff- Parkinson-White syndrome. Physical examination findings are nonspecific for PES, particularly if the patient is not experiencing a tachyarrhythmia. There are no specific laboratory findings for pre-excitation syndrome. Electrolyte abnormalities are commonly monitored and corrected in order to prevent or decrease the chance for arrhythmias.
Similarly, patients are usually screened with thyroid function tests which could indicate a potential treatable trigger for tachycardia. Delta wave slurred upstroke in the QRS complex due to fusion of early ventricular activation from pre-excitation via the accessory pathway with normal ventricular activation via the AV nodal pathway.
Presence or prior documentation of a tachyarrhythmia commonly seen in pre-excitation such as AVRT or atrial fibrillation with rapid ventricular rate RVR. It should be noted that although the wide and aberrated QRS complexes seen in patients with PES and atrial fibrillation may be similar or identical to those seen when in sinus rhythm, the width of the QRS complexes may vary and at times be normal due to a rate-related phenomenon.
No Delta wave present; QRS interval may appear normal or sometimes a left bundle-branch block pattern may be present. There are two types of AVRT based on the direction of the reentrant rhythm: orthodromic and antidromic. Diagnosis is made by comparing the QRS complexes showing pre-excitation seen during atrial fibrillation to those seen on baseline ECG while a patient is in sinus rhythm.
These are usually guided by the polarity of the Delta wave and the R- to S-wave relationship in the anterior or precordial leads of the ECG. Consultation with either a cardiologist or cardiac electrophysiologist is recommended in order identify the location of an AP and also diagnose PES. In controlled settings, adenosine adminstration is sometimes used as a diagnostic tool in order to unmask accessory pathways if there is no apparent retrograde conduction on ECG or if the pathway is concealed.
Procainamide or amjaline can be used as a challenge test to assess the refractoriness of antegrade conduction down the AP. There is a risk of AV block with the use of these drugs. Treadmill exercise testing can also be used to assess the risk for potential conduction down the AP or dangerous tachyarrhythmias. Electophysiologic studies may be used to both identify asymptomatic patients at risk for malignant tachyarrhythmias associated with the presence of an AP as well as confirm the presence of APs in patients with suspected PES.
Holter or event monitors are sometimes employed to record or document tachyarrhythmias in patients in whom there is a suspicion for both arrhythmias and pre-excitation. Other cardiac testing may be indicated based on the above results or findings, but the tests mentioned above are the recommended initial tests to be considered in the diagnosis and management of patients with PES. Immediate management steps in patients with PES include prompt diagnosis and rapid treatment of any life-threatening arrhythmias.
The first step in the immediate management of patients with PES and an associated tachyarrhythmia is determining whether or not the patient is considered to be stable.
Advanced cardiac life support guidelines exist for management of both stable and unstable tachycardia. The following will discuss management tips specific to inpatients with PES who develop stable tachycardia. Patients experiencing an acute tachyarrhythmia should be placed on telemetry with serial vital sign measurements. Supplemental oxygen should also be considered in certain patients. An ECG should be completed to help determine what type of arrhythmia the patient is experiencing.
Continuous ECG monitoring or rhythm strips may be needed to assess the immediate effect of certain treatments. In some cases, stable patients should be connected to a defibrillator with defibrillator pads in the event they become unstable or if cardioversion is needed. Patients should have a functioning intravenous IV catheter in place in order to effectively administer drugs as needed. If available, electrolytes and thyroid function should be reviewed or sent for analysis in order to correct any abnormalities which may have triggered or contributed to the arrhythmia.
Likewise, any other possible triggers of tachyarrhythmia e. Treatment is also different depending on the type of tachyarrhythmia present. Unstable tachycardia should be treated with emergent electrical cardioversion. For stable tachycardia, vagal maneuvers or pharmacologic treatment may achieve the desired goals in management. There is recent evidence to suggest that postural modification to the Valsalva maneuver may be more effective than the standard Valsalva maneuver alone for the emergency treatment of supraventricular tachycardia.
In cases of stable tachycardia not responding to treatment with pharmacologic or noninvasive means, cardioversion may have to be considered. In patients who are stable and in whom cardioversion is being used, sedatives and anesthetic agents should be administered prior to cardioversion if possible. Pharmacologic treatment has two purposes in the treatment of patients with PES and an associated tachyarrhythmia. First, some medications can reduce certain factors that may induce tachycardia in these patients.
Second, some medications target the weaker limb of the reentrant circuit either the AV node or the AP , which generally has a longer refractory period and is less conductive.
Thus, in orthodromic AVRT without pre-excitation on baseline ECG concealed accessory pathway , or with pre-excitation pattern if other antiarrhythmics have failed, maneuvers and drugs that block the AV node by either increasing its refractory period or decreasing conduction along the tract are recommended. These include vagal maneuvers, carotid massage, IV adenosine, beta blockers, and calcium-channel blockers. IV digoxin is not typically used in the immediate management of this arrhythmia given its delayed onset of action and risk of ventricular fibrillation.
AV nodal agents in general carry an inherent risk of increased conduction via the accessory pathway if the rhythm spontaneously degenerates to atrial fibrillation. IV procainamide is another option to use as it prolongs refractoriness and decreases conduction in most all cardiac tissues. Thus, procainamide can also block conduction down the AP. Procainamide is typically used for this reason in the acute treatment of patients with known AP or in those whom the diagnosis is unclear and the fear of AV nodal blockade leading to dangerous conduction down the AP exists e.
AV nodal blockade should be avoided though, as the RVR seen in the setting of atrial fibrillation in cases of degeneration to atrial fibrillation or misdiagnosis can be transmitted via the AP, therefore increasing the risk of life-threatening ventricular fibrillation. Thus, AV nodal blockers such as beta blockers, calcium-channel blockers, adenosine, and digoxin should not be used to treat new antidromic AVRT as it may lead to accelerated tachycardia, degeneration into atrial fibrillation, or even ventricular fibrillation.
It should also be entertained that some patients may have multiple APs and retrograde conduction may actually be occurring via another AP and not the AV node. As mentioned above, conduction in antidromic AVRT occurs antegrade down the AP and in most cases retrograde via the normal conduction system unless multiple APs exists. In cases where antidromic AVRT has previously been documented or known to exist in a patient with pre-excitation, the arrhythmia should be treated as ventricular tachycardia or an unknown wide complex tachycardia.
Wide complex tachycardia is treated with synchronized cardioversion in unstable patients and sometimes in stable patients if control cannot be achieved with antiarrhythmic drugs. Medications recommended for the treatment of wide complex tachycardia include IV procainamide, sotalol, amiodarone, or lidocaine in patients with a structurally normal heart. Amiodarone or lidocaine can be used in patients with structurally abnormal hearts or known decreased LVEF. The wide complex tachycardia in antidromic AVRT is typically monomorphic.
It should be noted that although the QRS complexes are usually wide and aberrated compared to those seen when the patient is in sinus rhythm, the width of the QRS complexes may vary and at times be normal due to a rate-related phenomenon.
In patients with known pre-excitation or PES, or in those where it is unknown or if there is no baseline ECG showing pre-excitation while in sinus rhythm but the suspicion is high, a rhythm control strategy is recommended for atrial fibrillation. There is no single clear first-line agent, but options include the class III antiarrhythmic ibutilide or the class IA antiarrhythmic procainamide, both of which are available IV.
Procainamide is recommended if ibutilide is not available or if there is significant concern for prolonged QT interval which may occur with ibutilide. Amiodarone is another IV antiarrhythmic that may come to mind because it is safe in patients with heart failure and decreased LVEF. It should be noted, however, that amiodarone is not approved for the acute control of atrial fibrillation in patients with PES, and, notably, has beta blocking effects and may increase ventricular response.
Amiodarone therefore should not be used IV for acute control of pre-excited atrial fibrillation. In addition to amiodarone, AV nodal blocking agents such as IV beta blockers, calcium-channel blockers, digoxin, and adenosine are also contraindicated in patients with PES and atrial fibrillation. Any of these medications may accelerate the ventricular rate and cause ventricular fibrillation.
It should also be noted that patients who have been in atrial fibrillation for greater than 48 hours or of unknown duration should be anticoagulated if able before undergoing rhythm control or cardioversion. Use of antiarrhythmic agents which may convert patients in atrial fibrillation to sinus rhythm e. The physical exam is extremely important in helping determine which patients are considered to have stable versus unstable tachycardia and thus what acute treatment algorithm should be used.
Patients who are hemodynamically unstable, especially if they have signs or symptoms of hypoperfusion, should be treated following ACLS protocol and typically undergoing immediate electrical cardioversion. For all patients with PES, identification and then elimination of possible triggers of tachyarrhythmias is advised.
For asymptomatic patients with PES, the overall low risk of sudden cardiac death and supraventricular tachycardia argue against routine invasive management. Noninvasive exercise testing or procainamide challenge may be used to help risk-stratify patients and can be done in a step-wise fashion prior to invasive testing. Noninvasive testing is especially useful for identifying low-risk patients. A high-risk patient identified by EP study may then undergo catheter ablation.
Ablation of the AP should be considered in other patients with pre-excitation, particularly if they are at high risk for developing malignant tachyarrhythmias. This also should be considered in patients who have high risk professions, are athletes, or have a family history of sudden cardiac death. Invasive testing and treatment with EP and catheter-based ablation is usually considered to have a low risk for complications, especially at experienced treatment centers.
Regardless, complications do occur and each patient should be evaluated individually on the appropriateness for testing and treatment based on their history and goals of care.
The type of approach and ablation strategy varies depending on the location of the accessory pathway, the number of pathways present, and also the preferred mode of treatment by the electrophysiologist. Typically, EP studies with ablation occur using a catheter with sheath and endovascular approach. Epicardial pathways do exist which may require a percutaneous or surgical approach.
In rare cases, a surgical approach for ablation may be needed in certain patients who fail other approaches or treatment. These medications are usually given as a single, higher-dose administration than that used for chronic maintenance therapy to prevent arrhythmias.
This strategy in suitable patients decreases the long-term side effects and toxicities associated with chronic medication use and may in some cases decrease the medical costs for the patient. Whether used as chronic maintenance therapy or pill-in-the-pocket, first-line medications include oral class IC antiarrhythmic drugs such as flecainide or propafenone. Second-line medications include class III agents dofetilide or sotalol.
Class IA drugs such as quinidine, procainamide, and disopyramide may also be useful. Other drugs used in the chronic prevention of orthodromic AVRT in patients with PES include oral beta blockers second-line in low-risk patients , non-dihydropyridine calcium-channel blockers, amiodarone if refractory to other agents , and digoxin not recommended as monotherapy. Long-term management of antidromic AVRT in patients with PES should focus on ablation, reserving medical management for patients who refuse, are unable to undergo, or are refractory to ablation.
Therapies include class IC medications as first-line such as oral flecainide or propafenone. Second-line medications include class IA drugs such as quinidine, procainamide, and disopyramide.
Amiodarone is another second-line therapy for the treatment of antidromic AVRT in patients with PES but should be used with caution due to its AV nodal blocking properties. In Wolff-Parkinson-White syndrome, antegrade conduction occurs over an accessory pathway.
If atrial fibrillation, develops this is a medical emergency as very rapid ventricular rates can develop. See also Overview of Arrhythmias Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope.
Atrial thrombi may form Patients have sudden episodes of palpitations that begin and If atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary If atrial fibrillation, develops this is a medical emergency as very rapid ventricular rates can develop Patients with concealed WPW syndrome are not at risk because in them, antegrade conduction does not occur over the accessory connection.
Ventricular response is very fast RR intervals minimum of msec. Shortly thereafter, ventricular fibrillation develops lead II continuous rhythm strip at bottom.
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