PROPIO DE LOS SANTOS ENERO

14.3.1 – SVT: What is the Rhythm?

The patient is a hemodynamically stable adult who presents to the ED with the rhythm below. The QRS is confirmed to be narrow on 12-lead ECG.

What is the Rhythm?

Clinically – What should you do next?

Figure 14.3.1-1: The patient is stable. What is the rhythm likely to be? What next? 14.3.2 – What is the Rhythm in Figure 14.3.1-1?

The rhythm in Figure 14.3.1-1 is rapid and regular. We are told that a 12-lead ECG confirms QRS narrowing in all leads. The rate is just under 200/minute. No P waves are seen. We have therefore described a regular SVT without clear sign of normal atrial activity. This description should bring to mind LIST #2 of the 3 entities to especially consider in the differential diagnosis of a regular SVT (Table 14.3.2-1):

Because the rate of the regular SVT in Figure 14.3.1-1 is very rapid (well over 160/minute) — PSVT (Paroxysmal Supra-Ventricular Tachycardia) is the most likely diagnosis.

Table 14.3.2-1: Common causes of a regular SVT rhythm when sinus P waves are not clearly evident. (NOTE: We previously presented this Table in Section 13.6).

As discussed in Section 13.6 – our purpose in suggesting use of LIST #2 is that in our experience, one of the 3 entities on this list will turn out to be the diagnosis for 90-95% of regular SVT rhythms when normal sinus P waves are not seen (automatic atrial and junctional tachycardias are far less common – esp. if the patient is not digoxin-toxic).

Calculation of the rate of the regular SVT may then provide invaluable assistance for determining etiology.

PEARL: Use of the Every-other-Beat Method (first discussed in Section 02.9) — facilitates calculation of heart rate when the rhythm is regular and the rate is fast. Pick a QRS that begins on a heavy line (as does the S wave for the 6th beat in Figure 14.3.1-1). Measure the R-R interval for every-other-beat — which is just over 3 large boxes. Thus, half the rate in Figure 14.3.1-1 is just under 100/minute — which means the actual rate is a bit below 200/minute (we estimate ~190/minute).

The rhythm in Figure 14.3.1-1 provides an excellent example of how to narrow down one’s differential diagnosis for the SVT rhythms:

The fact that this SVT rhythm is regular — essentially rules out AFib and MAT as possibilities. This leaves us with the 3 most common causes of a regular SVT to contemplate: i) Sinus

tachycardia; ii) Atrial flutter; and iii) PSVT (Table 14.3.2-1).

Children may attain sinus tachycardia rates of 200/minute or more. A young adult (in their 20s or 30s) may attain sinus tachycardia rates of ~180/minute or more during vigorous exercise (ie, running a 100-yard dash). Outside of those situations – it is unlikely for a patient presenting for medical attention to have sinus tachycardia at rates over 160-170/minute. It is also highly unlikely for AFlutter to present with a rate of 190/minute (which is too slow in an untreated patient for AFlutter with 1:1 AV conduction – and too fast for AFlutter with 2:1 AV conduction). This is why PSVT is almost certainly the diagnosis of the rhythm in Figure 14.3.1-1.

IF the rate of the regular SVT in Figure 14.3.1-1 were slower (say, closer to 150-160/minute) — then we would not be able to distinguish between the above 3 entities. This is the case in Figure 14.3.3-1:

Figure 14.3.3-1: Regular SVT without sign of normal sinus P waves. Because the rate of this regular SVT is ~150/minute – Any of the 3 entities in LIST #2 (Table 14.3.2-1 ) might be present. Although we suspect PSVT (since we see neither sinus P waves nor indication of flutter waves) – there is no way to be certain of the diagnosis from this single monitoring lead. As a result – sinus tachycardia,

atrial flutter and PSVT should all be considered in the differential diagnosis. Other means (ie, medication, a vagal maneuver) will be needed to clarify the diagnosis (See text).

14.3.4 – KEY Clinical Points: Regarding PSVT

PSVT is a regular supraventricular tachycardia that most often occurs at a rate of between 150-to- 240/minute. Atrial activity is usually not evident — although subtle notching or a negative deflection (representing retrograde atrial activity) may at times be seen at the end of the QRS. Mechanistically — PSVT is a reentry tachycardia that almost always involves the AV node ( ergo the other name for this rhythm = AVNRT = AV Nodal Reentry Tachycardia).

The impulse continues to circulate within the AV node until the reentry pathway is either interrupted (ie, by AV nodal blocking drugs or a vagal maneuver) — or until it stops spontaneously (Figure 14.3.4-1).

Figure 14.3.4-1: The mechanism of PSVT is AV nodal reentry (ergo the term AVNRT that is also used to designate this rhythm). It can be seen from this figure that each time the impulse completes the reentry circuit – retrograde conduction (back to the atria) as well as forward conduction to the ventricles (through the His-Purkinje system) occurs. This retrograde conduction back to the atria can sometimes be seen on the ECG during tachycardia (See text).

14.3.5 – PSVT: The Clinical Importance of Reentry

Awareness of reentry as the mechanism in PSVT is important diagnostically and therapeutically. It means that the arrhythmia is likely to be self-perpetuating unless/until something happens to interrupt the cycle.

Think of 50 young children holding hands and running around in a circle. If someone sticks out their foot to trip one of the children – it is likely that all of the children will fall down… So it is with reentry. Interruption of the cycle for the briefest of moments (by an AV-nodal-blocking drug or a vagal maneuver) may be enough to break the cycle and convert the rhythm.

14.3.6 – PSVT: Use of a Vagal Maneuver

Use of a vagal maneuver may be helpful diagnostically and therapeutically in management of the SVT rhythms. Consider Figure 14.3.6-1 which is continuation of the rhythm shown in Figure 14.3.1-1 at

the start of this section.

What happens to the regular SVT rhythm in the beginning of Figure 14.3.6-1 after the red arrow when CSM (Carotid Sinus Massage) was applied?

Is this an expected response?

HINT: Feel free to refer back to Section 13.10 regarding the usual response of SVT rhythms to vagal maneuvers.

Figure 14.3.6-1: What happens after CSM (arrow)? Is this an expected response? (See text). ANSWER to Figure 14.3.6-1:

PSVT typically responds to vagal maneuvers with either abrupt conversion to sinus rhythm – or – there is no response at all …

Abrupt conversion to sinus rhythm is seen shortly after CSM is applied in Figure 14.3.6-1.

Do not be alarmed if several ventricular beats are initially seen right after a vagal maneuver. This almost always rapidly resolves.

Realize that a vagal maneuver will not always work for PSVT. It is not uncommon for nothing to happen – in which case trial of an AV nodal rate-slowing drug may be in order (See Section 14.3.9).

Sometimes reapplication of a vagal maneuver after administration of rate-slowing medication may be effective, whereas the vagal maneuver had no effect prior to giving the drug.

14.3.7 – Beyond-the-Core: Recognizing Retrograde P Waves with PSVT

As a more advanced facet of this topic – Consider the situation in Figure 14.3.7-1. This 12-lead ECG was obtained from a hemodynamically stable patient with “palpitations”. A regular SVT rhythm at ~150/minute is seen. Normal sinus P waves are absent (ie, there is no upright P wave preceding each QRS complex in lead II). Instead – retrograde atrial conduction indicative of reentry is present. Do you the retrograde P waves?

Which leads in Figure 14.3.7-1 manifest retrograde atrial activity during the tachycardia? How does recognition of retrograde atrial activity in this example help you clinically?

Figure 14.3.7-1: Regular SVT at ~150/minute. Which leads manifest retrograde P waves during the tachycardia? (See text).

ANSWER to Figure 14.3.7-1

As illustrated by Figure 14.3.3-1 – the differential diagnosis of a regular SVT at ~150/minute without normal sinus P waves includes the 3 entities in LIST #2 (Table 14.3.2-1 ): i) Sinus tachycardia; ii) Atrial flutter; and iii) PSVT. When no atrial activity at all is seen ( as was the case in Figure 14.3.3.-1) – then the rhythm could be any of these 3 entities.

Retrograde P waves are seen in many leads in Figure 14.3.7-1. We highlight some of these

retrograde P waves by red arrows in Figure 14.3.7-2. Specifically – negative retrograde P waves are clearly seen in each of the inferior leads (II,III,aVF). Negative retrograde P waves account for angulation in the ST segment just prior to ascent of the T wave in lead V3 (red arrow) – and

probably also in V4,V5,V6. In addition – positive retrograde P waves are clearly seen in leads aVR and V1 (red arrows), and possibly also in aVL and V2.

Figure 14.3.7-2: Red arrows highlight retrograde atrial activity that was present in Figure 14.3.7-1. Retrograde P waves are seen in virtually all leads in this tracing, except perhaps for lead I (See text).

Clinically – the importance of recognizing retrograde atrial activity is twofold:

It solidifies the diagnosis of reentry as the mechanism for the regular SVT rhythm in Figure 14.3.7- 1. Knowing that P waves come after the QRS (not before) – and knowing there is only one P wave for each QRS rules out sinus tachycardia and AFlutter – thus confirming PSVT as the diagnosis. Awareness of reentry as the mechanism for this regular SVT rhythm facilitates decision-making for management (Section 14.3.9).

14.3.8 – Way Beyond-the-Core: Distinction Between AVNRT vs AVRT

Up until now – we have preferentially used the term, “PSVT” (Paroxysmal SupraVentricular Tachycardia) to designate regular SVT rhythms with reentry as their underlying mechanism. The word “paroxysmal” was chosen because of the common sudden onset of these tachycardias (often precipitated by a PAC, PJC, or PVC occurring at just the right moment in the cardiac cycle to initiate a circuit of self-perpetuating reentry in or around the AV node). This reentry was schematically illustrated in Figure 14.3.4-1.

A more accurate terminology distinguishes between AVNRT (AV Nodal Reentry Tachycardia) - in which the reentry circuit is contained within (or just next to) the AV node – vs AVRT

(AtrioVentricular Reciprocating Tachycardia) – in which the reentry circuit extends further away outside of the AV nodal area to the vicinity of the atrioventricular valvular rings over an AP

(Accessory Pathway).

We have already discussed AVRT in Section 12.7 under the various SVT pathways in patients with WPW. The “good news” – is that most of the time it does not matter clinically in the acute situation whether the true mechanism of PSVT is AVNRT (reentry over a small circuit within the AV node in a patient who does not have WPW) – vs – AVRT (reentry that extends outside the AV node involving a longer circuit that travels over an AP in a patient with WPW). This is because initial treatment measures are the same for AVNRT and AVRT when the QRS complex is narrow.

Longterm management of the patient with AVRT may differ from that for AVNRT in certain regards. Patients with AVRT have an accessory pathway. There is therefore potential for sudden onset of very rapid supraventricular rates if these patients develop atrial fibrillation or flutter (Sections 12.8, 12.9). In addition – patients with WPW who develop PSVT (AVRT) may occasionally manifest QRS widening with this supraventricular tachycardia if conduction is

antidromic (first down the AP) instead of orthodromic (down the AV nodal-His-Jurkinje system – then retrograde up the AP). As discussed in Section 12.10 – On those rare occasions when this happens, the QRS will be wide and the PSVT rhythm may be indistinguishable from VT. BOTTOM Line: Suspecting the presence of a concealed AP in a patient who presents with PSVT may lower one’s threshold for referral to an EP cardiologist. Ablation of the AP is usually curative.

We contrast the usual ECG picture of narrow-complex AVNRT vs AVRT in Figure 14.3.8-1. Red arrows highlight retrograde atrial activity in selected leads as previously discussed in Section 14.3.7.

What is the difference in the R-P’ interval highlighted by the red arrows – compared to the R-P’ interval for the blue arrows within the inserts of leads II, aVR and V1?

Clinically – In which case (red or blue arrows) would you suspect AVRT as the mechanism? In which case would you suspect AVRT?

Figure 14.3.8-1: A final look at the regular SVT rhythm previously shown in Figure 14.3.7-2 – with addition of inserts for leads II, aVR and V1. What is the difference between red and blue arrows in the R-P’ interval? (See text).

ANSWER to Figure 14.3.8-1:

The R-P’ interval (ie, retrograde distance between the QRS complex and the retrograde P wave that follows) – is clearly shorter for the P waves highlighted by the blue arrows:

PSVT due to AVNRT typically has a very short R-P’ interval (blue arrows). This is because the reentry circuit is contained either within or right next to the AV node. As a result – there is less distance for the impulse to travel during the reentry cycle. This is by far the most common situation for PSVT – in which retrograde atrial activity is either completely hidden within the QRS complex during tachycardia, or at most notches the most terminal aspect of the QRS (as it does for the blue arrows in Figure 14.3.8-1).

In contrast – narrow-complex AVRT in a patient with WPW is more likely to manifest a longer R- P’ interval (red arrows in Figure 14.3.8-1). This is due to the longer distance the impulse must travel from the AV node to the AP during the reentry cycle.

Clinical “Take-Home” Points: Although the various mechanisms of AVNRT and AVRT rhythms are complex (clearly extending Beyond-the-Core for many ACLS providers) – Recognition of retrograde atrial activity during narrow-complex PSVT rhythms is not difficult once made aware of what to look for. Figure 14.3.8-1 compares the two common situations. In either case –

recognition of retrograde P waves during PSVT confirms reentry (and rules out sinus

tachycardia and atrial flutter) as the mechanism for the tachycardia. This facilitates initial clinical decision-making in treatment (Section 14.3.9). Beyond-the-Core: Recognition that the R-P’ interval during PSVT is longer than expected (extending to the middle of the ST segment) suggests there may be a concealed AP. Our threshold for EP referral of such patients is lower.

PEARL: It is good practice to always obtain a 12-lead ECG after conversion of PSVT to sinus rhythm. Doing so sometimes facilitates retrospective detection of “telltale” retrograde atrial activity that may not have been readily apparent during tachycardia (by carefully comparing the terminal portion of the QRS complex and ST-T wave during and after the tachycardia).

FINAL Note: Other types of reentry supraventricular tachycardias exist (beyond the scope of this ePub). These include sophisticated fast-slow AVNRT, in which the retrograde P wave is negative in lead II with a very long R-P’ interval. Suffice it to say that initial treatment measures discussed in Section 14.3.9 are usually effective in the acute situation.

14.3.9 – PSVT: Acute Treatment Priorities

Although PSVT may occur in any population – it is often seen in otherwise healthy individuals. Patients with PSVT will almost always be hemodynamically stable (exceptions include older patients with significant underlying heart disease and persistent PSVT). As a result — medical treatment will usually be effective in the acute situation. Electrical cardioversion is only rarely necessary.

Consider initial use of a vagal maneuver if no contraindications (ie, Do not do carotid massage in an older patient, especially if a carotid bruit is heard). Some patients with PSVT are highly

responsive to vagal maneuvers (See also Sections 13.8 and 13.10).

Adenosine — is a drug of choice for PSVT (and for SVT of uncertain etiology that occurs in an ED or hospital setting). Give 6mg IV by rapid IV push (over 1-3 seconds!) — followed by a fluid flush. IF no response in 1-2 minutes — a 2nd dose (of 12mg) may be given. (See also Sections 13.13 and 13.14 for more on use of Adenosine for SVT rhythms).

The half-life of Adenosine is very short (less than 10 seconds) — so PSVT may recur. As a result — consider the need for starting the patient on a longer-acting drug.

Other options for treatment of PSVT include Diltiazem (IV bolus and/or drip) – or Verapamil – or a β-blocker (IV or PO). Selection of one of these agents may be made for PSVT or SVT of

uncertain etiology that either occurs in- or out of the hospital. Oral forms of these drugs are used for PSVT that occurs in an ambulatory setting (See Sections 13.15 and 13.6 for details on dosing). Use of an anxiolytic (ie, a benzodiazepine) — will often be helpful as an adjunct. In addition to attenuating anxiety that so often accompanies this highly symptomatic arrhythmia — anxiolytics may reduce sympathetic tone (thereby slowing conduction down over a portion of the reentrant

pathway).

Once the patient has been converted to sinus rhythm — Minimize or eliminate potential precipitants (ie, caffeine; alcohol; cocaine; amphetamines; OTC sympathomimetic drugs including cough-cold preparations and diet pills — as well as psychological stress). 14.3.10 – PSVT: Longterm Treatment Considerations

Many patients with PSVT will experience recurrence of this arrhythmia. In some – episodes are infrequent. In others – PSVT may recur often. This brings up the issue of longterm management. Although complete discussion of this topic extends beyond the scope of this ePub – several basic concepts regarding longterm treatment issues can be stated:

Identification and elimination of precipitating factors may sometimes be all that is necessary. The most common “culprit” is caffeine – but other potential precipitants include over-the-counter sympathomimetics (including cough-cold preparations and diet pills), amphetamines, alcohol, cocaine, and psychologic stress.

necessarily needed, especially in patient who only have infrequent episodes.

In patients who continue to have frequent PSVT recurrence despite attempts at addressing potential precipitating factors – daily use of an AV nodal blocking drug (diltiazem, verapamil, a beta- blocker) may be indicated. The dose required to minimize episodes may be titrated for each

individual patient. Surprisingly – no more than a very low dose of a beta-blocker may be all that is needed to prevent PSVT recurrence in patients for whom sympathetic tone plays a prominent

causative role.

Maintenance therapy need not be daily in those patients who only have intermittent episodes every few months. Instead, in selected appropriate cases — such patients may be able to stay at home and take a single dose of an AV nodal blocking drug plus a benzodiazepine at the onset of an episode (thereby often avoiding the need to go to the ED).