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Intraventricular conduction abnormalities
Normally, the entire mass of ventricular myocardium is depolarized in about 80 to 100 milliseconds. This requires highly synchronous electrical activation of the ventricular myocardium, which can be achieved only through the rapidly conducting His-Purkinje system (HPS). The term intraventricular conduction disturbances (IVCDs) refers to abnormalities in the intraventricular propagation of supraventricular impulses resulting in changes in the morphology and/or duration of the QRS complex. These changes in intraventricular conduction can be fixed and present at all heart rates, or they can be intermittent (transient). They can be caused by structural abnormalities in the HPS or ventricular myocardium, functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction), or ventricular preexcitation over a bypass tract.
Transient bundle branch block
The term aberration is used to describe transient bundle branch block (BBB) and usually does not include persistent QRS abnormalities caused by persistent BBB, preexcitation, or the effect of drugs. Transient BBB can have several mechanisms, including acceleration-dependent block, pause-dependent block, and concealed conduction. These mechanisms of aberration can occur anywhere in the HPS, and, unlike in chronic BBB, the site of block during aberration can shift. Right bundle branch block (RBBB) is the most common pattern of aberration, perhaps in part due to the thin nature of its anatomy, occurring in 80% of patients with aberration and in up to 100% of cases of aberration in normal hearts.
Acceleration-dependent bundle branch block
Conduction velocity depends, in part, on the rate of rise of phase 0 (dV/dt) of the action potential and the height to which it rises. These factors, in turn, depend on the membrane potential at the time of stimulation. At more negative membrane potential, more sodium (Na + ) channels are available for activation, allowing for a greater influx of Na + into the cell during phase 0 and, hence, larger action potential amplitude, fast depolarizing Na + current, and faster conduction velocity.
On the other hand, when stimulation occurs during phase 3 of the action potential, before full voltage recovery and at less negative transmembrane potentials, a portion of Na + channels is still refractory and unavailable for activation. Consequently, the Na + current (I Na ) and slope of phase 0 of the action potential are reduced, and the resulting action potential has slower conduction properties and is more susceptible to conduction block ( Fig. 11.1 ).
Phase 3 block (also called voltage-dependent block) occurs when an impulse arrives at tissues that are still refractory due to incomplete repolarization. Functional or physiological phase 3 aberration can occur in normal fibers if the impulse is sufficiently premature to encroach on the physiological refractory period of the preceding beat. This is commonly seen with a premature atrial complex (PAC) with a very short coupling interval that attempts to depolarize the HPS during phase 3 of the action potential and, hence, is conducted aberrantly, most often with RBBB.
Manifestations of phase 3 block include BBB and fascicular block, as well as complete atrioventricular (AV) block. Transient left bundle branch block (LBBB) is less common than RBBB (only 25% of phase 3 aberration is of the LBBB type). The block usually occurs in the very proximal portion of the right bundle (RB). Phase 3 block constitutes the physiological explanation of several phenomena, including aberration caused by premature excitation, Ashman phenomenon, and acceleration-dependent aberration.
Importantly, in the presence of HPS disease, the mechanism of acceleration-dependent aberration may no longer be related to phase 3 block. In this setting, aberration can be precipitated by premature or shorter-coupled impulses occurring well after the completion of phase 3 of the action potential. This type of block or aberrancy is usually a sign of conduction system disease. In normal myocardial cells, the recovery of electrical excitability coincides in time with voltage recovery, that is, the end of the action potential. The resting membrane potential remains polarized throughout diastole. In contrast, under pathologic conditions (e.g., ischemia, hyperkalemia, hypoxemia, acidosis), cardiomyocytes can have a less negative resting membrane potential. Hence, a portion of Na + channels remains closed and unavailable for activation throughout diastole. This results in reduced upstroke velocity and smaller amplitude of the action potential. At more depolarized resting potentials, the Na + current cannot be activated, though a strong stimulus can still induce a “slow response” action potential carried out by the slowly depolarizing calcium current. The “slow response” is characterized by slow conduction properties and refractoriness that can extend beyond the end of the action potential, a phenomenon known as postrepolarization refractoriness ( Fig. 11.1 ). As a result, a premature stimulus occurring during the early phase of diastole may fail to trigger a propagating action potential and, hence, manifest as block or aberration. Furthermore, the diseased HPS cells with depressed resting membrane potential are vulnerable to the phenomenon of concealed conduction and rate-dependent repetitive conduction block (see below), which can also mediate, at least in part, acceleration-dependent block.
Aberration caused by premature excitation
Premature excitation can cause aberration by encroaching on the refractory period of the bundle branch prior to full recovery of the action potential, namely during the so-called voltage-dependent refractoriness (see Fig. 5.30 ). In normal hearts, this type of aberration is almost always in the form of RBBB ( Fig. 11.2 ), whereas such aberration in the abnormal heart can manifest as either RBBB or LBBB.
At normal heart rates, the effective refractory period (ERP) of the RB exceeds that of the atrioventricular node (AVN), His bundle (HB), and left bundle (LB). At faster heart rates, the ERP of both bundle branches shortens; however, RB ERP shortens to a greater degree than LB ERP, so the duration of the refractory periods of the two bundles crosses over, and LB ERP becomes longer than that of the RB. This explains the tendency of aberration to be in the form of RBBB when premature excitation occurs during normal heart rates and in the form of LBBB when it occurs during fast heart rates.
Ashman phenomenon
The Ashman phenomenon refers to aberration occurring when a short cycle follows a long one (long-short cycle sequence) ( Fig. 11.3 ). Aberrancy is caused by the physiological changes of the conduction system refractory periods associated with the R-R interval. Normally, the refractory period of the HPS lengthens as the heart rate slows and shortens as the heart rate increases, even when heart rate changes are abrupt. Thus, aberrant conduction can result when a short cycle follows a long R-R interval. In this scenario, the QRS complex that ends the long pause (i.e., long R-R interval) is conducted normally but creates a prolonged ERP of the bundle branches. If the next supraventricular impulse approaches the bundle branches after a short coupling interval, it may be conducted aberrantly because one of the bundles is still refractory as a result of a lengthening of the refractory period following the immediately preceding QRS (phase 3 block). RBBB aberration is more common than LBBB in this setting because at heart rates usually present, the RB has a longer ERP than the LB.
The Ashman phenomenon can occur during second-degree AV block (see eFig. 10.5 ), but it is most common during atrial fibrillation (AF, in which it was originally described), whereby the irregularity of the ventricular response results in frequently occurring long-short cycle sequences. Of note, aberration caused by the Ashman phenomenon can persist for several cycles. The persistence of aberration can reflect a time-dependent adjustment of refractoriness of the bundle branch to the abrupt change in cycle length (CL), or it can be the result of concealed transseptal activation (see later).
The aberrancy can be present for one beat and have a morphology resembling a premature ventricular complex (PVC), or it can involve several sequential complexes, mimicking ventricular tachycardia (VT). In the setting of aberrancy during AF, the mere “long-short cycle sequence” characteristic of the Ashman phenomenon may not be helpful in differentiating aberration from ventricular ectopy. Although a long cycle (pause) sets the stage for the Ashman phenomenon, it also tends to precipitate ventricular ectopy. Furthermore, concealed conduction occurs frequently during AF, and therefore it is never possible to know from the surface ECG exactly when a bundle branch is activated. Thus, if an aberrant beat does end a long-short cycle sequence during AF, it can be because of the refractoriness of a bundle branch secondary to concealed conduction into it rather than because of changes in the length of the ventricular cycle.
Nevertheless, there are several features of ventricular ectopy that can help distinguish a PVC from an aberrantly conducted QRS complex (“Ashman beat”) during AF ( Table 11.1 ). PVCs are usually followed by a longer R-R cycle, indicating the occurrence of a compensatory pause, the result of retrograde conduction into the AVN and anterograde block of the impulse originating in the atrium. Hence, the presence of consistently long R-R cycles after the aberrated beats is suggestive of PVCs. A ventricular origin is also likely when there is a fixed coupling cycle between the normal and aberrant QRS complexes. Additionally, the absence of aberrancy despite the presence of comparable long-short cycle sequences elsewhere in the rhythm recording argues against aberrancy and is more consistent with ventricular ectopy. Finally, QRS morphology inconsistent with LBBB or RBBB aberrancy argues against aberration and is consistent with ventricular origin of the QRS complex ( Fig. 11.4 ).
TABLE 11.1
Distinguishing Aberrantly Conducted Complexes From Premature Ventricular Complexes During Atrial Fibrillation
| ABERRATION | PREMATURE VENTRICULAR COMPLEXES | |
|---|---|---|
| Onset sequence | Long-short | Short-long |
| Rate parity between periods of wide vs narrow QRS complexes | Similar rates | Different rates |
| Coupling intervals from prior narrow QRS complexes | Variable over several occurrences | Same or similar over several occurrences |
| Regularity of consecutive wide QRS complexes | Irregular | Relatively regular |
| Fusion complexes | Absent | May be present |
Aberration caused by heart rate acceleration
As the heart rate accelerates, the HPS refractory period shortens, allowing for normal 1:1 conduction at the faster atrial rate. However, refractoriness of the HPS eventually reaches a critical value beyond which it can no longer shorten in response to a further increase in the atrial rate; at this point, BBB or AV block may occur. Acceleration-dependent BBB is a result of failure of the action potential of the bundle branches to shorten in response to acceleration of the heart rate ( Fig. 11.5 ). As noted previously, the ERP of the RB normally shortens at faster heart rates to a greater degree than that of the LB; this finding explains the more frequent RBBB aberration at longer CLs (i.e., at slower heart rates) and LBBB aberration at shorter CLs.
Notably, during slowing of the heart rate, intraventricular conduction often fails to normalize at the critical CL, and aberration persists at cycles longer than the critical cycle that initiated the aberration. Once acceleration-dependent BBB is established, the actual cycle for the blocked bundle does not begin until approximately halfway through the QRS complex because of concealed transseptal conduction (see later); thus, it is necessary for the heart rate to slow down more than would be expected to reestablish normal conduction (i.e., slower than the rate at which aberration first appeared).
Occasionally, with increasing heart rate or persistence of fast heart rate, acceleration-dependent aberration can disappear. The normalization of a previously aberrant QRS complex can be explained by the shortening of the ERP of the bundle branches to a greater degree than that of the AVN, by a time-dependent gradual shortening of the refractory period of the affected bundle branch (a phenomenon occasionally referred to as “restitution”), or by the loss of transseptal concealed conduction.
Importantly, acceleration-dependent aberration is a marker of a diseased HPS when it (1) appears at relatively slow heart rates (less than 70 beats/min); (2) displays LBBB ( Fig. 11.6 ); (3) appears after several cycles of accelerated but regular rate; or (4) appears with gradual rather than abrupt acceleration of the heart rate.
Pause-dependent bundle branch block
Pause-dependent (or bradycardia-dependent) block occurs when the conduction of an impulse is blocked in tissues well after their normal refractory periods have ended. Phase 4 aberration is one explanation for the development of aberration at the end of a long cycle (i.e., after a pause). Phase 4 block is governed by the same physiological principles as those for phase 3 block. Membrane responsiveness is determined by the relationship of the membrane potential at excitation with the maximum rate of rise of phase 0. The availability of the Na + channels is reduced at less negative membrane potentials, and activation at a reduced membrane potential is likely to cause aberration or block. The cause of membrane depolarization (i.e., reduction of membrane potential) in the setting of phase 4 block, however, is different from that in phase 3 block.
Phase 4 or diastolic depolarization of the action potential is a property of pacemaker cells of the heart; normal His-Purkinje fibers do not possess this property at rates faster than 40 beats/min; however, diseased Purkinje cells can acquire the property of phase 4 depolarization at more rapid rates. Enhanced phase 4 depolarization within the bundle branches can be caused by enhanced automaticity or partial depolarization of injured myocardial tissue. In this setting, the maximum diastolic potential immediately follows repolarization, from which point the membrane potential steadily depolarizes (becomes less negative). This reduction in membrane potential, in turn, causes the inactivation of some Na + channels. Thus, an action potential initiated early in the cycle (immediately after repolarization) would have a steeper and higher phase 0 and, consequently, better conduction than would an action potential initiated later in the cycle when the membrane potential at the time of the stimulus is reduced, with resulting slower upstroke velocity and smaller amplitude of the action potential and, hence, slower conduction or block ( Fig. 11.7 ). Phase 4 aberration is “pause dependent” because the pause allows for spontaneous depolarization and, hence, the cell is activated from a less negative potential, and the result is impaired conduction ( Fig. 11.8 ). The critical prolongation of the input stimulus is typically initiated by a compensatory pause after a PAC or PVC, spontaneous slowing of the sinus rate, or overdrive suppression of sinus rhythm upon the termination of a fast supraventricular rhythm. Once such a critical diastolic membrane potential is reached (at which Na + channel inactivation occurs), subsequent conduction may no longer resume until a well-timed escape beat or premature beat (sinus or ectopic) resets the transmembrane potential to its excitable state. The extent of depolarization has to be significant, because lesser amounts of depolarization improve excitability (membrane voltage closer to the threshold voltage) and should improve conduction.
Despite the fact that bradycardia is common and cells with phase 4 depolarization are abundant, phase 4 block is not commonly seen in normal myocardial tissue. In fact, most reported cases are associated with structural heart disease. One explanation for this phenomenon is that in normal fibers, conduction is well maintained at membrane potentials more negative than −70 to −75 mV. Significant conduction disturbances are first manifested when the membrane potential is less negative than −70 mV at the time of stimulation; local block appears at −65 to −60 mV. Because the threshold potential for normal His-Purkinje fibers is −70 mV, spontaneous firing occurs before the membrane can actually be reduced to the potential necessary for conduction impairment or block. In fact, in the latter setting, mild membrane depolarization can actually improve conduction because the membrane potential is moved closer to the threshold potential. Phase 4 block is therefore pathological when it does occur, and it requires one or more of the following: (1) the presence of slow diastolic depolarization, which needs to be enhanced (i.e., occurring at rates faster than these cells normally spontaneously depolarize); (2) a decrease in excitability (a shift in threshold potential toward zero) so that, in the presence of significant bradycardia, sufficient time elapses before a new stimulus arrives, thus enabling the bundle branch fibers to reach a potential at which conduction is impaired; and (3) a deterioration in membrane responsiveness so that significant conduction impairment develops at −75 mV instead of −65 mV; this occurrence would also negate the necessity for such a long cycle before conduction fails. Also, it is important to recognize that, in some cases, pause-dependent aberrancy may be caused by other mechanisms (e.g., source-to-sink mismatch) that may not be related to phase 4 depolarization.
Pause-dependent or phase 4 block almost always manifests an LBBB pattern, likely because the left ventricular (LV) conduction system is more susceptible to ischemic damage and has a higher rate of spontaneous phase 4 depolarization than the right ventricle (RV). Both acceleration-dependent and pause-dependent aberrancy can be seen in the same patient with an intermediate range of CLs associated with normal conduction. The prognosis of rate-dependent BBB largely depends on the presence and severity of the underlying heart disease. Its clinical implications are not clear, and it usually occurs in diseased tissue and in the setting of myocardial infarction (MI), especially inferior wall MI.
Aberration caused by concealed transseptal conduction
Concealed transseptal conduction likely underlies aberration occurring in several situations, including the perpetuation of aberrant conduction during tachyarrhythmias, unexpected persistence of acceleration-dependent aberration, and alternation of aberration during atrial bigeminal rhythm.
Perpetuation of aberrant conduction during tachyarrhythmias
During a supraventricular tachycardia (SVT) with normal ventricular activation, a PVC originating from the RV can retrogradely activate the RB early, whereas retrograde activation of the LB occurs later, following transseptal conduction of the PVC. Consequently, although the RB ERP expires in time for the next SVT impulse, the LB remains refractory because its actual cycle began later than the RB. Therefore, the next SVT impulse traveling down the HB encounters an excitable RB and a refractory LB; thus, it propagates to the RV over the RB (with an LBBB pattern, phase 3 aberration). Conduction subsequently propagates from the RV across the septum to the LV. By this time, the distal LB has recovered, allowing for retrograde penetration of the LB by the SVT impulse propagating transseptally, thereby rendering the LB refractory to each subsequent SVT impulse ( Fig. 11.9 ). This process is repeated, and the LBBB pattern continues until another well-timed PVC preexcites the LB (and either “peels back” or shortens its refractoriness) so that the next impulse from above finds the LB fully recovered ( Fig. 11.5 ).
More commonly, a PAC blocks anterogradely in the proximal portion of the RB to cause RBBB, conducts down the LB to activate the ventricle, and crosses the septum to excite the RB retrogradely and make it refractory for the next supraventricular complex, thus perpetuating the RBBB (see below).
Unexpected persistence of acceleration-dependent aberration
As noted, acceleration-dependent BBB develops at a critical rate faster than the rate at which it disappears ( Fig. 11.10 ). This paradox is most commonly ascribed to concealed conduction from the contralateral conducting bundle branch across the septum with delayed activation of the blocked bundle. Such concealed transseptal activation results in a bundle branch-to-bundle branch (RB-RB or LB-LB) interval shorter than the manifest R-R cycle. The reason is that the actual cycle for the blocked bundle does not begin until approximately halfway through the QRS complex, because it takes 60 to 100 milliseconds for the impulse to propagate down the RB and transseptally reach the blocked LB. Consequently, for normal conduction to resume, the cycle (R-R interval) during deceleration must be longer than the critical cycle during acceleration by at least 60 to 100 milliseconds.
However, unexpected delay of normalization of conduction cannot always be explained by concealed conduction. Conduction sometimes normalizes with slowing of the heart rate, only to recur at cycles that are still longer than the critical cycle. Such a sequence excludes transseptal concealment as the mechanism of recurrence of the aberration. Similarly, when the discrepancy between the critical cycle and the cycle at which normalization finally occurs is longer than the expected transseptal activation time (approximately 60 milliseconds in the normal heart and 100 milliseconds in the diseased states), transseptal concealment alone cannot explain the delay ( Fig. 11.10 ). Fatigue and overdrive suppression have been suggested as possible mechanisms of the delayed normalization of conduction.
Alternation of aberration during atrial bigeminal rhythm
A bigeminal rhythm can be caused by atrial bigeminy, 3:2 AV block, or atrial flutter with alternating 2:1 and 4:1 AV conduction. The alternation can be between a normal QRS complex and BBB or between RBBB and LBBB.
When alternation occurs between a normal QRS complex and RBBB during atrial bigeminy, the ERP of both RB and LB starts simultaneously following the normally conducted PAC, and the ERP of both branches is relatively short because of the preceding short cycle. After the pause, the sinus beat conducts normally, and the ERP of both bundle branches starts simultaneously but is relatively long because of the preceding long cycle. However, because the RB ERP is relatively longer than that of the LB, the next PAC encroaches on the RB refractoriness and conducts with an RBBB pattern (phase 3 block). Subsequently, that PAC is conducted down the LB and across the septum. The PAC activates the RB retrogradely after some delay (concealed transseptal conduction), so the RB-RB interval (during the following pause) and the RB ERP become shorter. As a result, by the time the next PAC reaches the RB, the RB is fully recovered because of its abbreviated ERP (reflecting the shorter preceding RB-RB interval, which is shorter than the manifest R-R interval during the preceding pause), and normal conduction occurs.
The same phenomenon (concealed transseptal conduction) explains alternating RBBB and LBBB during bigeminal rhythms. In the presence of RBBB, transseptal concealed conduction from the LB to the RB shortens the RB-RB interval relative to the now longer LB-LB interval. As a result, the ERP of the LB is longer and conduction in the LB fails. In the presence of a refractory LB, conduction propagates through the RB. The delayed transseptal activation of the LB shortens the LB-LB interval. The ERP of the RB is now relatively longer, because RB conduction is blocked.
Chronic bundle branch block
Anatomy and physiology of the His-Purkinje system
Cardiac skeleton
The cardiac skeleton consists of four rings of dense connective tissue that surround the mitral and tricuspid valves and extend to the origins of the aorta and the pulmonary trunk. The aortic valve occupies the central position with the other valve rings attached to it. The right fibrous trigone is formed by the triangular junction between the aortic valve and the medial parts of the tricuspid and mitral valves, and it represents the largest thickening and strongest portion of the cardiac skeleton (see Fig. 22.3 ). Together with the membranous septum, the right fibrous trigone constitutes the central fibrous body. The membranous interventricular septum is an inferior extension of the central fibrous body that attaches to the muscular interventricular septum. The membranous septum is crossed on its right aspect by the attachment of the tricuspid valve, dividing the septum into AV and interventricular components. The electrically inert central body and skeleton of the heart functions to electrically isolate the atria from the ventricles, except at the site of penetration of the AV conducting system.
His bundle
The HB connects with the distal part of the compact AVN and penetrates the central fibrous body (where it is called the nonbranching or penetrating bundle) in a leftward direction (away from the right atrial endocardium and toward the crest of the muscular interventricular septum) ( eFig. 11.1 ). The HB then emerges on the crest of the ventricular septum and continues sandwiched between the muscular and the membranous components of the septum for 1 to 2 cm before dividing into the RB and LB. Viewed from the aorta, the HB passes beneath the part of the membranous septum that adjoins the interleaflet fibrous triangle between the right and noncoronary sinuses. The HB is insulated from the atrial myocardium by the membranous septum and from the ventricular myocardium by connective tissue of the central fibrous body, thus preventing atrial impulses from bypassing the AVN. Proximal cells of the penetrating portion are heterogeneous and resemble those of the compact AVN; distal cells are larger, similar to cells in the proximal bundle branches and ventricular myocytes.
Right bundle
The RB travels as a direct continuation of the HB down the right side of the interventricular septum toward the RV apex. The RB is a narrow, cable-like structure, insulated by a fibrous sheath from surrounding myocardium and remains without ramifications for most of its length until it approaches the origin of the right anterior papillary muscle, where it divides profusely into a network of subendocardial fascicles spreading to the RV septal and free walls ( eFig. 11.1 ). Additionally, free-running strands extend from the RB toward the apical trabeculated portion of the RV. The ventricular cavity is also bridged via connections through the moderator band (a muscular structure that crosses from the septum to the RV free wall and supports the anterior papillary muscle of the tricuspid valve). The RB runs subendocardially in its basal and apical thirds and deeper within the muscular portion of the septum in the middle third. This path renders the subendocardial segments vulnerable to stretch and trauma.
Left bundle
The LB at its origin is not a discrete branch of the HB but arises as numerous fine, intermingling fascicles that leave the left margin of the branching HB through most of its course along the crest of the muscular ventricular septum. The predivisional portion of the LB penetrates the membranous portion of the interventricular septum under the aortic ring and then divides under the septal endocardium into two branches: the left anterior fascicle (LAF) and the left posterior fascicle (LPF). An estimated 65% of individuals have a third fascicle of the LB, the septal or left median fascicle (LMF). The fascicles cascade down the LV septum in a fan-like configuration with extensive interconnections. Unlike the cord-like RB, the LB and its divisions are diffuse, fan-like structures that branch out just beyond their origin ( eFig. 11.1 ). The LAF represents the superior (anterior) division of the LB, the LPF represents the inferior (posterior) division, and the LMF represents the septal (median) division.
The LB subdivisions extend to the mid portion of the septum before they detach from the underlying endocardium and form free-running false tendons that traverse the ventricular chamber, projecting predominantly toward the papillary muscles. The fascicles become ramified in the ventricular apex and extend back along the ventricular walls toward the cardiac base.
The LAF crosses the anterobasal LV region toward the anterior papillary muscle and terminates in the Purkinje system of the anterolateral LV wall. The LPF appears as an extension of the main LB and is large in its initial course. It then fans out extensively toward the posterior papillary muscle and terminates in the Purkinje system of the posteroinferior LV wall. The LMF runs to the interventricular septum; it arises in most cases from the LPF, less frequently from the LAF, or from both, and in a few cases it has an independent origin from the central part of the main LB at the site of its bifurcation.
Purkinje fibers
The bundle branches and fascicles consist of bundles of Purkinje cells insulated from the surrounding myocardium by a dense sheath of connective tissue. Insulation is lost distally as the Purkinje network connects the ends of the bundle branches to the ventricular myocardium. This design enables the transfer of action potentials to the ventricular apex first before activating the ventricular myocardium at the base, ensuring a synchronized and coordinated apex-to-base contraction pattern that optimizes ventricular ejection.
A combination of subendocardial and free-running Purkinje fibers (false tendons) form complex three-dimensional mesh-like networks on the endocardial surface of both ventricles and penetrate only the inner third of the myocardium. Purkinje fibers tend to be less concentrated at the base of the ventricles and at the tips of the papillary muscle. The free-running false tendons traverse the ventricular chamber and reattach at the free wall myocardium, projecting predominantly toward the papillary muscles. This pattern promotes septal-free wall synchronization.
Cardiac Purkinje cells exhibit structural and electrophysiological (EP) features that are distinct from nodal and working cardiomyocytes. Purkinje fibers are larger than working cardiomyocytes and are often larger and more rod-shaped than sinus and AV nodal cells. Additionally, Purkinje cells have fewer myofibrils, which are different in composition of myosin from the cells of working myocardium. These myofibrils function only as passive cytoskeletal components. Purkinje cells contain a considerable amount of glycogen, and they exhibit more resistance to hypoxia than ventricular myocardium cells. As compared to the working ventricular cardiomyocytes, the action potential in Purkinje fibers has a faster upstroke velocity (dV/dt), higher amplitude, more prominent early phase of rapid repolarization (phase 1), more negative plateau potential, and significantly longer duration.
The Purkinje fiber network is critical for the almost simultaneous depolarization of the terminal HPS and propagation of the cardiac impulse to the entire RV and LV endocardium. Purkinje cells are specialized to conduct rapidly, at 2.3 m/sec, much faster than working ventricular cardiomyocytes (0.75 m/sec). This rapid conduction is facilitated by the high expression of Na + channels, resulting in action potential upstroke velocities of ∼1000 V/sec. Additionally, an exceptionally high enrichment of connexin proteins (Cx40, Cx43, Cx45) results in a very low intercellular resistance (as low as 100 ohms/cm). Purkinje fibers are connected to the working myocardial cells by intercalated disks. One Purkinje fiber transfers the impulse to thousands of ventricular cardiomyocytes.
The Purkinje fiber network arrangement guarantees a synchronous action of working cardiomyocytes during the contraction. Ventricular activation starts at the left side of the interventricular septum, followed by a wave of excitation traveling from the apex to the base (to ensure efficient and optimized ejection toward the basally located semilunar outlet valves), and from the endocardium to the epicardium.
Blood supply
The HB and predivisional portion of the LB receive dual blood supply from the septal branches of the anterior and posterior descending coronary arteries. The RB and LAF are supplied by the septal perforating branches of the left anterior descending coronary artery. The LPF is supplied by the conus branch of the right coronary artery in the majority of cases. Hence, RBBB or LAF block can result from occlusion of the left anterior descending artery, whereas the development of LBBB during acute MI usually indicates occlusion of both the right and the left anterior descending coronary arteries.
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