Electrical
Conduction System In The Heart
Electrical conduction in
cardiac muscle (Figure 13a) Cardiac muscle cells are connected via intercalated discs (see
Chapter 2). These incorporate regions where the membranes of adjacent cells are
very close, called gap junctions. Gap junctions consist of proteins
known as connexons, which form low-resistance junctions between cells.
They allow the transfer of small ions and thus electrical current. As all cells
are therefore electrically connected, cardiac muscle is said to be a functional
(or electrical) syncytium. If an action potential (AP) is initiated
in one cell, local currents via gap junctions will cause adjacent cells to
depolarize, initiating their own AP. A wave of depolarization will therefore be
conducted from cell to cell throughout the myocardium. The rate of conduction
is partly dependent on gap junction resistance and the size of the
depolarizing current. This is related to the upstroke velocity of the AP
(phase 0). Drugs that slow phase 0 therefore slow conduction (e.g.
lidocaine, class I antiarrhythmics). Pathological conditions such as ischaemia
may increase gap junction resistance, and slow or abolish conduction.
Retrograde conduction does not normally occur because the original cell is
refractory (see Chapter 11). Transfer of the pacemaker signal from the sinoatrial
node (SAN) and synchronous contraction of the ventricles is facilitated by conduction
pathways formed from modified muscle cells.
(Figure 13b)
Sinoatrial node
The heart beat is normally initiated in the SAN, located at the
junction of the superior vena cava and right atrium. The SAN is a ∼2-mm-wide
group of small elongated muscle cells that extends for ∼2 cm down the
sulcus terminalis. It has a rich capillary supply and sympathetic and
parasympathetic (right vagal) nerve endings. The SAN generates an AP about once
a second (sinus rhythm, Figure 13c; see Chapter 11).
The impulse spreads from the SAN across the atria at ∼1
m/s. Conduction to the atrioventricular node (AVN) is facilitated by larger
cells in the three internodal tracts of Bachmann (anterior), Wenckebach
(middle) and Thorel (posterior).
The atria and ventricles are separated by the non-conducting annulus
fibrosus. The AVN marks the upper region of the only conducting route
through this band. It is similar in structure to the SAN, situated near the
interatrial septum and mouth of the coronary sinus, and innervated by
sympathetic and left vagal nerves. The complex arrangement of small cells and
slow AP upstroke (see
Chapter 11) result in a very slow conduction velocity (∼0.05
m/s). This provides a functionally significant delay of ∼0.1 s between
contraction of the atria and ventricles, reflected by the PR interval of the electrocardiogram (ECG; see
Chapter 14). Sympathetic stimulation increases conduction velocity and reduces
the delay, whereas vagal stimulation slows conduction and increases the delay.
Bundle of His and Purkinje system
The bundle of His transfers the impulse from the AVN to the top of
the interventricular septum. Close to the attachment of the tricuspid septal
cusp it branches to form the left and right bundle branches. The
left bundle divides into the posterior and anterior fascicles. The bundles
travel under the endocardium down the walls of the septum, and at the base
divide into the multiple fibres of the Purkinje system. This distributes
the impulse over the inner walls of the ventricles. Cells in the bundle of His
and Purkinje system have large
diameters (∼40 µm) and rapid AP upstroke, and consequently fast
conduction (∼4 m/s). The impulse spreads from the Purkinje cells
through the endocardium towards the epicardium at 0.3–1 m/s, thereby initiating
contraction.
Abnormalities of impulse generation or conduction (see also
Chapters 48–50)
Sinus tachycardia (100–200 beats/min) is normal in exercise
or excitement, but also occurs when pathological stimuli (e.g. phaeochromocytoma,
heart failure, thyrotoxicosis) elevate sympathetic tone and accelerate SAN
firing. Sinus tachycardia generally starts and stops gradually. Treatment, if
required, involves removing the underlying cause. The ECG is otherwise normal.
Conversely, sick sinus syndrome, generally caused by SAN fibrosis,
causes slowed impulse generation and bradycardia (slow heart rate), or a
sustained or intermittent failure of the impulse to reach the AVN, termed sinoatrial
block (Figure 13i). Because other parts of the conduction system also
exhibit pacemaking activity (see Chapter 11), sick sinus syndrome can result in
the emergence of escape beats or rhythms in which impulses arising
elsewhere (usually the AVN) can activate ventricular depolarization. Sick sinus
syndrome can be treated by implantation of a pacemaker.
Heart block Abnormally slow conduction in the AVN can
result in incomplete (first-degree) heart block (AV block; Figure
13d), where the delay is greater than normal, resulting in an extended PR
interval. Second-degree heart block occurs when only a fraction of
impulses from the atria are conducted; for example, ventricular contraction is
only initiated every second or third atrial contraction (2:1 or 3:1 block;
Mobitz II; Figure 13e). Wenckebach block (Mobitz I) is another type of
second-degree block, in which the PR interval progressively lengthens until
there is no transmission from atria to ventricles and a QRS complex is missed;
the cycle then begins again (Figure 13f). Patients with first or second- degree
block are often asymptomatic. Complete (third-degree) heart block occurs
when conduction between atria and ventricles is abolished (Figure 13g,h). This
can result from ischaemic damage to nodal tissue or the bundle of His. In the
absence of a signal from the SAN, the AVN and bundle of His can generate a
heart rate of ∼40 beats/min (see Chapter 11). Some ventricular cells
spontaneously generate APs, but at a rate less than 20/min.
Bundle branch block When one branch of the bundle of His
does not conduct (left or right bundle branch block), the part of the
ventricle that it serves will be stimulated by conduction through the
myocardium from unaffected areas. As this form of conduction is slower,
activation is delayed and the QRS complex broadened, often with a more
prominent Q wave (Figure 13j).
