From the basic "conduction road map" of the heart, seen in Figure 1, we can start illustrating concepts.
|Figure 2: The sinoatrial node depolarizes and the depolarization wavefront travels rapidly along the internodal pathways and Bachmann's Bundle, towards the atrioventricular node and the left atrium.|
Beginning in Figure 2 and continuing through Figure 4, we can see the propagation of a depolarization wavefront started in the sinoatrial node and its eventual path through to the bundle branches. While difficult to express on an actual whiteboard, fading of the older impulses is used to help represent the time component of the signal.
Reentrant TachycardiasThe beauty of this style of drawing is the ability to convey concepts such as Atrioventricular Nodal Reentry Tachycardia (AVNRT). A certain subset of the population has two or more distinct zones of conduction in their AV node. Often there are dual pathways with one of the zones conducting impulses quickly but recovering slowly, and the other conducting impulses slowly and recovering quickly.
In a sinus rhythm this difference in conduction through the atrioventricular node is not apparent. However, if a well timed premature atrial contraction (PAC) is present, this dichotomy can be exploited. In Figure 5 we can see the sinus impulse arriving at the AV node, with part of the wavefront traveling through the fast pathway, and part of the wavefront traveling through the slow pathway.
Continuing in Figure 6, the slow pathway with its shorter effective refractory period, begins recovering quicker than the fast pathway. Once through the AV node the depolarization wavefront continues through the Bundle of His and into the bundle branches and Purkinje fibres as during normal conduction.
|Figure 6: The dichotomy of recovery in the two atrioventricular nodal pathways are illustrated.|
It is at this vulnerable point that a well timed extrasystole can take advantage of the heterogeneous repolarization of the AV nodal pathways. Figure 7 depicts the initiation of a PAC which reaches the slow pathway while it is completely recovered and the fast pathway is still absolutely refractory.
In Figure 8 we can see the "rotation" of reentry initiated as the depolarization wavefront travels forward (antegrade) through the slow pathway and backwards up (retrograde) the fast pathway which has now recovered. Impulses are then distributed down through the Bundle of His each time the rotation through the slow pathway reaches the insertion of the Bundle of His. It is this reentry, best illustrated as a rotation, that not only initiates the tachycardia but sustains the tachycardia as well.
When viewing Figure 8, you may see why typical AVNRT results in a Pseudo-S wave in Lead II (Figure 9) and Pseudo-R' wave in Lead V1, as once the tachycardia begins the impulses are conducted to the atria retrogradely from the fast pathway. Ventricular depolarization continues as it would during normal conduction, using the normal ventricular conduction tissues for propagation.
|Figure 9: The Pseudo-S wave, highlighted in red, seen during typical atrioventricular nodal reentry tachycardia as the atria are depolarized retrogradely.|
Reentry Outside the AV NodeAtrioventricular nodal reentry is not the only means of reentrant tachycardias. Less than 1% of the population features an extra "exit" in their conduction road map, known as an Accessory Pathway (AP, featured in Figure 10) or an Accessory Bypass Tract.
Drs. Wolff, Parkinson, and White were the first to describe a series of patients featuring bundle branch blocks and a short PR intervals who suffered from paroxysms of tachycardias in the 1930's. However, it was not until the late 1940's that these abnormalities were isolated by Drs. Ohnell and Wood as bundles of conducting tissue which connected the atria and ventricles, independent of the AV node.
AV nodal tissue features the property of decremental conduction; simply stated, it acts as a speed bump slowing the conduction of a depolarization wavefront. The upper limit of atrioventricular conduction is often less than 220 Hz although this varies with age. Typical accessory bypass tracts do not feature decremental conduction and can often conduct both antegrade and retrograde signals in excess of 220 Hz.
The hallmark feature of an AP is pre-excitation of the ventricles. As sinus impulses arrive at both the AV node and the AP, illustrated in Figure 11 and Figure 12, the depolarization wavefront is slowed in the AV node but conducted without delay through the AP.
|Figure 11: A sinoatrial node depolarization travels towards the AV node and an Accessory Pathway (AP).|
Figure 12 shows that ventricular myocardium begins depolarizing as the AP terminates directly into ventricular tissue.
|Figure 12: The depolarization wavefront is conducted through both the AV node and the AP. However, the AP conducts the impulse without delay and begins depolarization of a portion of the ventricle not a part of the normal conduction network.|
In Figure 13, this direct connection to ventricles pre-excites some myocardium while normal conduction through the bundle branches from the AV node occurs.
|Figure 13: As depolarization of the ventricles continues, the two wavefronts meet. The fusion of these two wavefronts often mimics a bundle branch block.|
|Figure 14a: Comparison of the QRS morphology during a sinus rhythm and a sinus rhythm with pre-excitation through an accessory pathway.|
Reentry Using an Accessory PathwayIf pre-excitation were the only feature of an accessory pathway, Wolff-Parkinson-White would exist merely as a fascinoma. However, as previously noted, most accessory pathways are pathological featuring non-decremental antegrade and retrograde conduction.
This additional circuit may join with the AV node and be exploited by extrasystoles or heterogeneous repolarization. This class of tachycardias is known as Atrioventricular Reciprocating Tachycardia (AVRT) or the older Circus Motion Tachycardia (CMT).
Orthodromic ReentryAVRT is divided into two types based on the direction of travel in the circuit. Orthodromic AVRT occurs when the reentry is antegrade through the AV node then retrograde through the AP; thus conduction through the ventricles proceeds normally. An orthodromic circuit can be initiated by a premature ventricular contraction (PVC) or blocked antegrade conduction through the AP.
Figure 15 illustrates the arrival of a sinoatrial depolarization at both the AV node and the AP, with forward conduction through the AP blocked.
|Figure 15: A sinoatrial depolarization arrives at the atrioventricular node and an accessory pathway, finding the AP blocked.|
|Figure 16: Conduction proceeds normally through the AV node.|
|Figure 17: As the ventricles depolarize and conduction continues through the ventricles the wavefront finds that retrograde conduction through the AP is not blocked, contrary to antegrade conduction.|
Antidromic ReentryIn Antidromic AVRT, conduction of the reentry circuit begins antegradely through the accessory pathway and completes retrogradely through the atrioventricular node. Because ventricular depolarization does not begin with the normal ventricular conduction network, antidromic AVRT will present as a regular wide complex tachycardia due to slower propagation of ventricular depolarization.
As in orthodromic AVRT, an antidromic circuit can begin with an extrasystole or with blocked conduction. In Figure 19, a PAC travels forward through the atria entering an accessory pathway and is concurrently blocked by a refractory AV node.
|Figure 19: An atrial extrasystole finds the AV node refractory, however, is able to conduct antegrade through an accessory pathway into the ventricles.|
|Figure 20: Activation of the ventricular myocardium begins outside the conduction network and eventually reaches the AV node.|
|Figure 21: Retrograde depolarization of the AV node and atria occurs. The accessory pathway does not feature the decremental conduction seen in the AV node and is already completely repolarized.|
Atrial Fibrillation and Wolff-Parkinson-WhiteUnfortunately, reentry rhythms are not the only means of tachycardias utilizing an accessory pathway. If an automatic atrial focus were to have access to a non-decremental accessory pathway the results will be rapidly fatal. Many patients with Wolff-Parkinson-White will experience episodes of atrial fibrillation (AF). In atrial fibrillation, numerous atrial wavefronts are present producing cyclic rates of 400-800 Hz.
Atrial fibrillation and WPW is characterized by varying degrees of fusion between antegrade conduction of f-waves through the AV node and the AP. This is seen on the surface ECG as a rapid, grossly irregular tachycardia with alternating QRS morphologies ranging from narrow to very wide.
Figure 23 features atrial fibrillation wavefronts depolarizing the AV node and encountering a refractory accessory pathway.
|Figure 23: Atrial fibrillation with conduction through the AV node and blocked conduction through an AP.|
|Figure 24: Conduction through the bundle branches and Purkinje Fibres propagates normally and the continued f-waves are blocked at both the refractory AV node and AP.|
|Figure 25: Non-decremental antegrade conduction of f-waves from atrial fibrillation through an AP into the ventricles. These f-waves are limited in propagation only by the effective refractory period of the AP and ventricular myocardium.|
|Figure 26: Varying degrees of fusion occur as antegrade conduction proceeds through the AV node and AP.|
I hope my digital reproductions of Whiteboard Cardiology proved useful and drop me a line if you have ideas for other concepts in electrocardiography that would be simplified through line art.
All of these images are free to use and licensed Creative Commons Attribution-Share Alike 3.0, available for download on my Google Drive. The originals were created using Paint.Net.