We prefer dual chamber pacing for all valid indications but AAIR pacing remains a not so infrequently used option in our setup.


RV pacing provides life sustaining rhythm support and is the most critical lead of a pacing system. However more and more patients are getting paced for non-life threatening yet highly symptomatic sinus node dysfunction. Therefore functional pacing and maintenance of physiologic cardiac activation is a prime concern when pacing for sinus dysfunction. To enable such, atrial pacing has evolved to be an integral component of pacing for sinus node dysfunction.

As long-term RV pacing has been proven to be deleterious, it became unwise to pace the RV when the problem is in the sinus node. Therefore initial attempts to avoid RV pacing  was to pace only the atrium provided the AV nodal function was acceptable. This was the AAI mode. [ Atrial demand pacing]. Subsequent development of advanced sensor technology enabled physiologic rate adaptation mimicking natural sinus node activity and AAI became AAIR [ Rate adaptive Atrial Demand Pacing]. Atrial only pacing was possible only if the AV node was normal – otherwise had to pace the ventricle. On the west side of the Atlantic, the skepticism for atrial only pacing was high and this accelerated the development of dual chamber pacing systems which would pace both chambers based on the underlying pathology and rhythm.

Dual chamber systems introduced an important benefit – maintenance of AV synchrony. This enabled AV synchronized pacing for even AV nodal disease (e.g. complete heart block) in addition to sinus node dysfunction. The biggest perceived advantage of dual chamber pacing in sinus disease was that if the patient developed AV nodal disease, there would be synchronized pacing for ventricles too. Dual chamber pacing became very popular in North America and was the mode of choice for pacing for a wide variety of brady-arrhythmias except permanent slow AF. However the Europeans were skeptical of dual chamber pacing and until DANPACE shed light to the matter, atrial only pacing remained quite popular in Europe. DANPACE provided evidence base for justification of dual chamber pacing for sinus node dysfunction – for clinico-pathological reasons and economic reasons

Regardless of the above, dual chamber systems are still very expensive compared to single chamber systems (and there is a unresolved issue of risk of heart failure with pure sinus node dysfunction). Therefore in cost-constrained developing country environments such as ours, we still attempt AAIR pacing if feasible. Usually these patients are young patients with only sinus node dysfunction and have had a non – invasive workup to assess AV nodal function before pacing AAI. An intra-operative testing of AV nodal function determines the final mode of pacing (our protocol is given in the section on Atrial Lead Implantation)

With regard to the site of pacing, right atrial appendage (RAA) is the location of choice – mainly because its an easily accessible and stable place. We avoid the lateral atrial wall because of phrenic nerve capture and the inter-atrial septum is only very rarely used for pacing because almost always, a good site in the RAA can be found.

Reccomended Reading
  1. Kenneth A. Ellenbogen –  Clinical Cardiac Pacing, Defibrillation, and Resynchronization Therapy 4e.
    • Chapter 10 : Clinical Trials of Atrial and Ventricular Pacing Modes by Carsten W. Israel
  2. Fred M. Kusumoto – Cardiac Pacing for the Clinician 2e. –
    • Chapter 9  : Sinus Node Dysfunction  by Irene H. Stevenson, Paul B. Sparks, and Jonathan M. Kalman
    • Chapter 10 : Acquired Atrioventricular Block  by S. Serge Barold and Bengt Herweg

Implantation of Atrial Lead

The steps are
  • Have vascular access : Either the only sheath (for AAIR) or second sheath for a dual system
  • If dual – ventricle lead in place and finalized
  • Insert atrial lead and park in right atrium (as described for the ventricular lead)
  • Change the straight stylet with a appropriate J curved stylet
  • Negotiate the distal curved end of the lead to the Right Atrial Appendage under fluroscopic guidance
  • Check parameters and deploy active fix screw
  • Exchange stylet to a straight one and anchor the lead at the pocket after removing the sheath.

Firstly, the lead has to be parked in the RA. If the system is going to be only AAIR then, the existing sheath can be used to insert the lead as described here for ventricular pacing.  If it is a dual chamber system, an additional sheath has be in place as described here via an additional guide-wire as described here.

One potential place where brisk forcible insertion might cause problems is the SVC free wall: If the sheath is too much in, the tip will lie against the free wall of the SVC and the lead coming out of it will impinge on the wall creating a resistance. Therefore it is imperative that fluroscopic screening is done at the slightest resistance without pushing the lead blindly. If impinging, the whole sheath should be slightly withdrawn and the lead marched forward with about inch of stylet pulled out to make it floppy and fall down

Note : The atrial leads are usually shorter than the ventricular leads. For a given manufacturer, all pacing leads are electrically identical but differ in lengths to facilitate ventricular versus atrial pacing. However they are interchangeable (e.g. A longer ventricular lead can be used for atrial pacing vice versa). Medtronic, St Jude Medical and Vitatron have 58 cm leads for the ventricles and 52 cm leads for the atria. Biotronik has 60 cm leads for the ventricle and 53 cm leads for the atria

Each lead is accompanied by a one or two pre-formed J shaped stylets – these vary in size and stiffness. Therefore if a lead refuses to move into the appendage, a stylet with a smaller curve can be tried.

If one appreciates the shape of the lead which is given by the stylet) it can be easily figured out why it is dangerous to pull the stylet fast : It can lead to a lead out-migration through the appendage roof. If pulled fast, the J stylet tip provides force at the lead tip forcing it cranially against the appendage roof. Since the screw is already deployed, it gets further wedged in the muscle wall and if the site of anchoring has a thin wall, the deployed screw length is sufficient to reach out of the myocardium into the pericardium. The potential serious complication is bleeding to the pericardial space – but the usual symptom is central pricking sharp chest pain. Author has seen three such cases where symptoms rapidly resolved after re-positioning the atrial lead.

Unexplained central pricking type chest pain after atrial pacing should prompt lead re-positioning. On table echocardiography is recommended before and after lead re-positioning to exclude bleeding. If the patient is on anticoagulants or anti-platelets, they should be temporarily withheld if not absolutely necessary – even in the absence of acute pericardial bleeding – as delayed bleeding may occur. Such patients warrant a repeat echocardiograph before discharge


If the pacing is for pure sinus node dysfunction, AAIR pacing can be considered (although dual chamber pacing is preferred). To pace in AAIR, one has to be absolutely sure that there is no current AV nodal disease. We assess this in two ways – Non invasively with Holter and Exercise testing and invasively during implantation of device. If holter and exercise ECG shows only evidence of sinus node dysfunction, we plan for an AAIR system and do intra-operative reconfirmation of AV nodal function. The intra-operative method is described below.

AV Nodal Wenckebach Point : AV node has decremental conducting properties i.e. at progressively faster sinus rates, the conduction time over the AV node increases (with manifest PR prolongation) and after a certain rate, it begins to block the conduction of certain P waves. This occurs in a pattern where the PR interval progressively lengthens and suddenly fails to conduct a P wave. Soon after the blocked P the subsequent conducted P wave has a shorter PR interval than the last conducted P wave thus implying that the AV node recovered during the non -conducted P wave. This is similar to type 1 heart block (Wenckebach type) and the heart rate at which the first dropped beat occurred is termed the Wenckbach point (WBP)
AV nodal conduction is highly dependent on autonomic function. Increased vagal tone decreases conduction velocity and sympathetic stimulation increases conduction velocity. Although Wenchbach phenomenon occurs at fast heart rates, the phenomenon is often seen in healthy young physically fit adults during sleep as their vagal tone is high during sleep. AV nodal conduction is also influenced by drugs such as some calcium channel blockers, digoxin, beta blockers etc.
In purely sick sinus disease, the AV nodal conduction is assumed to be normal. For pre-operative planning, we mainly do a holter and if the holter does not show evidence of AV nodal disease (baseline PR prolongation, Non conducted Ps in awake state) we consider AAI pacing. The issue with exercise testing is that due to sinus node disease, most patients are unable to mount a good sinus response to exercise – hence are unable to do an exercise ECG – but rarely a patient may have good chronotropic competence and if physically capable, doing an exercise ECG may provide useful information.
If AAI is anticipated, following steps are taken
Placement of Lead

First, the lead is placed in the RAA and sensing is tested. (Active fixation is NOT depolyed). If sensing is ok, we proceed to test AV nodal conduction. (Note : If there is no sinus activity, the sensing cannot be performed and proceed to AV node testing)

Testing of AV Ndoal Conduction

The atrium is now paced with progressively fast heart rates starting with around 70 at 5V. The pacing mode should be AAI but if the lead is not stable or if sensing was an issue, AOO (asynchronous atrial pacing) mode pacing may be needed to get stable pacing. At lower rates, there should be 1:1 conduction (each paced P followed by QRS complex). The pacing rate is progressively increased in steps and the ECG is carefully observed for non conducted Ps. Markers on programmer screen are very helpful in this regard. When a non conducted P is seen to occur consistently at a given rate, this is take as the Wenckebach Point. Progressive PR lengthening sometimes can be difficult to see and the best surrogate way to confirm is by observing the PR interval of the beat just before the non conducted beat and the PR interval of first conducted beat after the non conducted beat. The latter should be shorter than the previous. The initial overall ratio might be high (10:1) and therefore it is important to observe for at least 10 seconds after increasing the paced rates – or otherwise you may miss a non conducted P – or wrongly attribute to a non-captured atrial pace as a block

Practical Tip : At high rates ( e.g. > 130) if the ECG is noisy or if the lead stability is precarious and you are seeing missed Ps  haphazardly, its best to switch to AOO mode. To further add clarity, watch the pulse oximeter trace and the rate of the trace to corroborate with your ECG findings.
  • If the Wenckbach point is more than 140 (i.e. no block occurs at 140 bpm of atrial pacing) – we assume that the AV node is normal and proceed with AAI pacing
  • If the Wenckbach point is between 120 – 140, the testing is repeated after an IV injection of 0.6 mg of atropine. The presumption here is that the patient’s vagal tone may be high because of sedation and atropine would mitigate it – enabling faster conduction, If the Wenckebach point increases > 140 after atropine, we conclude that the AV node is intrinsically normal and proceed with AAI pacing
  • If the Wenckebach Point is less than 120 bpm at baseline or fails to improve after atropine, we assume that the AV node has intrinsic conduction difficulties and switch to either DDD or VVI on availability of devices.
Active Fixation of Lead

Once the decision to pace in AAI mode is taken, the screw is deployed and the lead is actively fixed to the RA after checking atrial pacing threshold. If the decision was to switch to VVI mode, the stylet is withdrawn and a 3D stylet is used to pace the mid-septum. If the choice was DDD, we would deploy the screw and fix the lead in the RAA before gaining access for the ventricular lead. (Since one lead is already in, the sheath of this lead is removed only after the second vascular puncture is done)