Specialized excitatory and conduction properties of cardiac muscles

Cardiac muscles form the bulk of the heart. Normal cardiac muscle cells of the atria and ventricles are contractile. In addition to contractile property, normal cardiac muscle cells also conduct electrical signals to neighboring cardiac muscle cells through gap junctions. Therefore, a typical cardiac muscle cell serves two basic functions:

  1. Contraction
  2. Conduction of electrical impulses to neighboring cardiac muscle cells

Moreover, most cardiac muscle cells possess the two functional properties. However, a small fraction (approximately 2 %) of cardiac muscle cells does not contract; these cells specialize in generating action potential spontaneously for the contraction of the heart. These specialized muscle cells called pacemaker cells of the heart do not contract; their role is to generate electrical signals for rhythmic contraction of the heart. A heartbeat occurs every time a pacemaker sends out an electrical impulse.

Pacemaker cells confer a unique property to the heart: which is its ability to contract without any outside signal.

The heart requires no external nerve input to contract (cardiac muscle contraction is myogenic)


The contraction of heart is myogenic: meaning that the electric signals responsible for the contraction of cardiac muscles arise from a unit of the cardiac muscle themselves.

Sinoatrial node (sinus node)

Sinoatrial node is a small-flattened strip of specialized cardiac muscle cells located in the superior wall of the right atrium slightly below the opening of the superior vena cava. The specialized cardiac muscle cells, which constitute the sinoatrial (SA) node, are not contractile because they barely have contractile muscle filaments.

These specialized cardiac muscle cells called pacemaker cells of the heart generate electrical impulses without any nerve input whatsoever. This property of the cardiac muscle to contract spontaneously without any form of neural signals called automaticity. This means the heart can contract without any connection to another part of the body because the signals for its contraction originate within the heart muscle itself (i.e. cardiac contraction is myogenic).

Comparing pacemaker cells with contractile cardiac muscle cells


Pacemaker cells also called autorhythmic cells exhibit important anatomical and functional differences with normal contractile cardiac muscle cells.

Morphologically, pacemaker cells (autorhythmic cells) are smaller; about 3 to 5 µm in diameter compared to the diameter of surrounding atrial muscle cell that have diameter of 10 to 15 µm. Moreover, they contain just few contractile elements, consequently, they lack organized sarcomeres; this morphological difference accounts for an important functional difference between pacemaker cells and normal contractile cardiac muscle cells. Functionally, pacemaker cells are unable to contribute to the contractile force of the heart since they lack organized sarcomeres.

Despite the anatomical and functional differences between pacemaker (autorhythmic) cells and contractile cardiac muscle cells, pacemaker cells form part of the atrial syncytium and directly connect with contractile atrial muscle cells. The essence of this connection is to allow action potential that arise in the sinoatrial node to spread into the atrial muscle wall instantly.

Conduction and spread of excitation within the heart


The specialized cardiac muscle cells of the sinoatrial node generate impulses that spread across the muscle cells of both atria rapidly. These impulses cause both atria to contract together as a unit. The electrical impulses are unable to spread to the muscle cells of the ventricles because the connective tissue band at the AV junction does not conduct electrical impulses.

Another collection of specialized cardiac muscle cells occur close to the AV junction forming the AV node. AV node is a sensory tissue that picks up electrical impulses that arrive from the SA node. Three internodal fibers convey the electrical impulses from the SA node to the AV node. By the time the impulses arrive at the AV node, the atrial syncytium have already contracted forcing blood down into the ventricles through the AV valves. The blood fills the ventricles stretching the ventricular chambers.

From the AV node, the electrical impulses to contract travel down the intraventricular septum, mainly insulated from nearby muscle fibers of the ventricles. Once the impulses arrive at the apex of the heart, they emerge and cause the apex to contract first. From the apex, the impulses emerge further up along the ventricular free wall, this region of the heart contracts last.

The nature of the spread of excitation and subsequent contraction has a functional significance. It allows the contraction to begin at the apex and then spread upwards pushing blood into their respective arterial trunks through the semilunar valves.

Neural and hormonal factors modify myogenic heart contraction


Although pacemaker cells generate impulses for heartbeat by themselves, and the heart contracts without nerve input from the brain, pacemaker cells and heart rhythm are under the influence of the autonomic nervous system (ANS) and a hormone called adrenaline.

Neural impulses from the brain and hormonal factors can either accelerate or slow down the pace of self-excitation (myogenic contraction). The modification of heart rate is necessary in order to meet the different demand of the body at different states. Therefore, neural and hormonal signals modify and regulate heart rhythm in response to body needs.

Both parasympathetic and sympathetic fibers innervate the cardiac muscles at strategic points, including the SA node (pacemaker cells), AV node, and other muscles of the heart. Activation of the parasympathetic or the sympathetic nerve supply to the heart results in significant changes in the basic rhythm of the heart.

Sympathetic nerve fibers to the heart are cardio-excitatory and directly innervate the SA node. The sympathetic nerve fibers supplying the heart are activated when we face danger; a good example is the classical ‘flight or fight’ response.

Adrenaline: adrenaline, a hormone released by the endocrine gland called adrenal gland increases both the rate and force of contraction of the myocardium. Sudden danger, fear, and attack are the main conditions that stimulate the adrenal gland to release adrenaline into blood.

Moreover, the release of adrenaline (epinephrine) by the adrenal gland makes the heart and other body tissues to respond as if there are under sympathetic stimulation.

The effects of sympathetic stimulation of the heart are increased firing rate by pacemaker cells, which results in an increase in heart rate. Sympathetic nerves that innervate the heart also called accelerator nerve upon stimulation release the neurotransmitter, nor-epinephrine (nor-adrenaline) at the SA node to increase heart rate.

In addition to the SA node and AV node, sympathetic nerve fibers give off numerous branches that run on coronary blood vessels to innervate the walls of the two ventricles. Here, the sympathetic fibers increase the force of contraction of these chambers.

Parasympathetic nerves to the heart are cardio-inhibitory (i.e. reduces heart rate and force of contraction). Upon stimulation, parasympathetic fibers that innervate the heart release the neurotransmitter, acetylcholine at their nerve endings on the SA node to reduce heart rate. Acetylcholine slows heart rate by decreasing the rate of depolarization at the SA node. In addition to reducing rate of sinus rhythm, acetylcholine decreases the excitability of internodal fibers between the SA node and the AV node consequently, slowing transmission of electrical impulses into the ventricles.

Because of its cardio-inhibitory role, the parasympathetic nerve to the heart also called the decelerator nerve because of its cardio-inhibitory role mainly slows both excitability and impulse conduction across the AV junction but has little effect on force of contraction.

Strong vagal (parasympathetic) stimulation and ‘ventricular escape’


Strong stimulation of parasympathetic supply to the heart can make the rhythmic excitation of sinoatrial node to cease completely. Moreover, strong vagal stimulation can block completely, the transmission of signals from atria to ventricles through the AV node.

As electrical impulses from the atria no longer reaches the ventricles, the ventricles cease to beat for a short period lasting for 10 to 20 seconds. However, after a short while, some cardiac muscle cells along the length of the purkinje fibers along the ventricular septum assumes the role of ventricular pacemaker firing at a much slower rate of about 20 to 40 beats per minute. This phenomenon called ‘ventricular escape’ is particularly important in certain heart conditions.

The parasympathetic nerve supply to the heart innervates the SA and AV node mainly, with considerably few fibers innervating atrial and ventricular musculature. In contrast, the sympathetic nerve fibers to the heart innervate virtually all parts of the heart, with abundant fibers innervating the SA node, AV node, atrial musculature, and ventricular musculature.

In our next lecture on cardiovascular function, we shall discuss the ionic basis of the automatic electrical rhythmicity of the pacemaker cells of the sinoatrial node.

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