SNRTs measure spontaneous recovery of the sinus node after overdrive suppression. Rapid pacing is delivered from the high right atrium (HRA) near the SAN at different cycle lengths (CLs) (e.g., 600 ms, 500 ms, and 400 ms) for 30 sec. At each pacing CL, the recovery interval or uncorrected SNRT (interval from last pacing stimulus to first spontaneous sinus electrogram at the HRA catheter) is measured (normal <1400 ms).¹ The uncorrected SNRT is a function of 1) retrograde perinodal conduction, 2) sinus node automaticity (and, therefore, sinus CL), and 3) antegrade perinodal conduction. The corrected SNRT accounts for the sinus CL by subtracting it from the recovery interval (corrected SNRT = recovery interval − sinus CL; normal <550 ms).¹ The pacing CL and SNRT demonstrate an inverse relationship until a point where shorter pacing CLs cause paradoxical shortening of the SNRT because of pacing-induced entrance block into the perinodal zone. The peak pacing CL is the shortest pacing CL resulting in the longest SNRT and is longer for patients with SAN dysfunction. Secondary pauses after pacing termination are sinus intervals that are longer than the SNRT.² The total recovery time is the amount of time after pacing that is required for the sinus rate to return to baseline (normal <5 sec or 4-6 beats). While abnormal SNRTs are specific for SAN dysfunction, variable penetration of pacing stimuli into the perinodal zone affects its sensitivity. Atropine can either shorten SNRTs by improving SAN automaticity or paradoxically increase SNRTs by improving perinodal conduction.³ The clinical equivalent of abnormal SNRTs are prolonged post-conversion pauses following abrupt termination of atrial tachyarrhythmias (Fig. 1-1).

SACTs measure perinodal conduction after the SAN has been reset (but not suppressed) by pacing.⁴,⁵ With the Narula method, burst pacing is delivered just slightly faster (≤10 bpm) than the sinus rate. With the Strauss technique, single atrial extrastimuli scan sinus rhythm during diastole. Extrastimuli fall into one of four zones: 1) collision (compensation), 2) resetting, 3) interpolation, and 4) reentry, but only extrastimuli falling into the zone of resetting are analyzed. With either method, the return interval (time from the last stimulus to the first spontaneous sinus electrogram at the HRA catheter) is measured and is the summation of the retrograde conduction time from pacing site to SAN + sinus CL + antegrade conduction time from SAN to pacing site.
Assuming that conduction times to and from the SAN are equal, the SACT = (return interval − sinus CL)/2 (normal: 45-125 ms).¹ Poor or absent perinodal conduction causes prolonged SACT, the clinical equivalent of which is sino-atrial exit block (Fig. 1-2).

The IHR is a measure of sinus node automaticity when devoid of autonomic control. Autonomic blockade is achieved by propranolol (0.2 mg/kg at 1 mg/min) (sympathetic block) followed 10 min later by atropine (0.04 mg/kg over 2 min) (cholinergic block).⁶,⁷ After autonomic blockade, the sinus rate is measured and compared to the predicted IHR (predicted IHR = 118.1 − [0.57 × age]).⁸ An IHR that is less than the predicted IHR demonstrates intrinsic SAN disease. An IHR that is equal to the predicted IHR demonstrates lack of intrinsic SAN disease and implicates exaggerated autonomic tone for SAN dysfunction.

Carotid sinus hypersensitivity causes an exaggerated autonomic reflex in response to carotid sinus baroreceptor stimulation (Fig. 1-3). ⁹,¹⁰ It is associated with older age and organic heart disease. Gentle pressure on the carotid sinus (massage, stiff neck collars, tight neckties) triggers activation of baroreceptors located in the carotid bulb. Afferent nerve fibers travel from the baroreceptors via the glossopharyngeal nerve to the nucleus tractus solitarius (vasodepressor medullary region of the brain). The efferent limb of the reflex arc is the vagus nerve whose terminals richly innervate the SAN and AVN causing sinus pauses and/or AV block. Cardioinhibitory and vasodepressor responses are defined as ventricular asystole >3 sec and >50 mm Hg drop in systolic blood pressure, respectively.⁹,¹¹ Because cholinergic fibers innervate both the SAN and AVN, the combination of sinus slowing and PR prolongation before AV block suggests hypervagotonia (vagotonic AV block).

During programmed atrial extrastimulation, single extrastimuli (A₂) are delivered with progressively shorter (10 ms) coupling intervals after a pacing drive train (A₁). At coupling intervals beyond the relative refractory period (RRP), the AH interval remains constant (A₁H₁ = A₂H₂). When the coupling interval reaches the AVN RRP, the AH interval prolongs because of decremental conduction over the AVN. The longest A₁A₂ interval causing A₂H₂ > A₁H₁ defines the AVN RRP. At a critically short coupling interval, the AVN effective refractory period (ERP) is reached and conduction blocks in the AVN. The longest A₁A₂ interval causing block in the AVN (A₂ without H₂) defines the AVN ERP. The shortest H₁H₂ interval for a given A₁A₂ interval defines the AVN functional refractory period (FRP) (AVN function curves plot A₁A₂ versus A₂H₂ or A₁A₂ versus H₁H₂).

Rapid atrial pacing with progressively shorter CLs causes steady prolongation of the AH interval because of decremental AVN conduction. The point at which block occurs in the AVN defines its Wenckebach CL.

Pacing-induced infrahisian block can either be 1) physiologic (functional) or 2) pathologic.¹⁴ Physiologic pacing-induced infrahisian block results from functional refractoriness in healthy His-Purkinje tissue often triggered by long-short sequences at the onset of rapid atrial pacing (normal His-Purkinje ERP ≤450 ms) (Fig. 1-4).¹⁵ Because His-Purkinje refractory periods are directly related to sinus CL, abrupt onset rapid pacing during slow sinus rates facilitates physiologic infrahisian block. In contrast, pathologic pacing-induced intra- and infrahisian block

results from abnormal refractoriness in diseased His-Purkinje tissue and observed during incremental or longer pacing CLs (>450 ms) (Figs. 1-5 and 1-6).¹⁵

Adrenergic and cholinergic innervation of the AVN but not His-Purkinje system allows autonomic manipulation of the conduction system to identify the site of block. The AVN protects the His-Purkinje system from rapid atrial rates, and the evaluation of His-Purkinje system function is limited by the AVN FRP. Shortening AVN refractoriness by atropine or isoproterenol allows more atrial inputs to reach the His-Purkinje system. While atropine and isoproterenol improve intranodal AV block, it paradoxically worsens AV block in the His-Purkinje system (Fig. 1-7).¹⁶ Conversely, while CSM increases vagal tone
and worsens intranodal AV block, it slows the sinus rate and can improve AV block in the His-Purkinje system.

Procainamide slows His-Purkinje conduction by blocking Na channels and delaying the upstroke (phase 0) of its action potential. It can, therefore, be a provocative test of His-Purkinje function.¹⁷ While procainamide normally increases HV intervals by 15-20%, the following responses are abnormal: 1) HV increase by 100%, 2) HV >100 ms, 3) spontaneous secondand third-degree infrahisian block, and 4) pathologic pacinginduced infrahisian block not observed at baseline.¹⁵

The ECG clues providing a presumptive localization of the site of AV block are the 1) PR interval, 2) QRS width, 3) pattern of AV block, and 4) morphology of escape complexes. During AV block, long conducted PR intervals (>300 ms) and narrow QRS complexes favor block in the AVN, while normal or mildly prolonged PR intervals with bundle branch block (BBB) suggest block below the His bundle. The presence of normal or mildly prolonged PR intervals and narrow QRS complexes raises the possibility of block within the His bundle (Figs. 1-8 and 1-9). Escape QRS complexes that are identical to conducted QRS
complex originate above the bifurcation of the His bundle and localize block to either the AVN or His bundle. While the AVN exhibits decremental conduction, His-Purkinje conduction is typically “all or none.” Therefore, second-degree AV block (Mobitz type I or Wenckebach) suggests block in the AVN, particularly if the difference between the first and last PR interval of a Wenckebach sequence is large and the QRS complex is narrow. Rarely, however, diseased His-Purkinje tissue can exhibit decremental conduction, but the increment in PR interval before block is generally smaller. A Wenckebach pattern with only small increments in the PR interval and a narrow QRS complex suggests intrahisian Wenckebach (Fig. 1-9). A Wenckebach pattern in the setting of BBB especially when prolongation of the PR interval is accompanied by changes in QRS morphology indicates infrahisian Wenckebach because bundle branch conduction contributes to formation of both the PR interval and QRS complex (Figs. 1-10 and 1-11). In contrast, second-degree AV block (Mobitz type II) indicates block in the His-Purkinje system. While Mobitz type II block typically occurs in the setting of BBB, the presence of a narrow QRS complex indicates block within the His bundle (Fig. 1-9).

The presence of a His bundle electrogram localizes the site of AV block.