Autonomic Innervation of the Heart and Vasculature

The medulla, located in the brainstem above the spinal cord, receives sensory input from different systemic and central receptors (e.g., baroreceptors and chemoreceptors) as well as signals from other brain regions (e.g., hypothalamus). Autonomic outflow from the brainstem is divided principally into sympathetic and parasympathetic (vagal) branches. Efferent fibers of these autonomic nerves travel to the heart and blood vessels where they modulate the activity of these target organs.

The heart is innervated by vagal and sympathetic fibers. The right vagus nerve primarily innervates the SA node, whereas the left vagus innervates the AV node; however, there can be significant overlap in the anatomical distribution. Atrial muscle is also innervated by vagal efferents, whereas the ventricular myocardium is only sparsely innervated by vagal efferents. Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.

Cardiac function is altered by neural activation. Sympathetic stimulation increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects. Sympathetic and parasympathetic effects on heart function are mediated by beta-adrenoceptors and muscarinic receptors, respectively.

Sympathetic adrenergic nerves travel along arteries and nerves and are found in the adventitia (outer wall of a blood vessel). Varicosities, which are small enlargements along the nerve fibers, are the site of neurotransmitter release. Capillaries receive no innervation. Activation of vascular sympathetic nerves causes vasoconstriction of arteries and veins mediated by alpha-adrenoceptors.

Parasympathetic fibers are found associated with blood vessels in certain organs such as salivary glands, gastrointestinal glands, and in genital erectile tissue. The release of acetylcholine (ACh) from these parasympathetic nerves has a direct vasodilatory action (coupled to nitric oxide formation and guanylyl cyclase activation). ACh release can stimulate the release of kallikrein from glandular tissue that acts upon kininogen to form kinins (e.g., bradykinin). Kinins cause increased capillary permeability and venous constriction, along with arterial vasodilation in specific organs.

Cardiovascular Physiology Concepts

Richard E. Klabunde, Ph.D.

Abnormal Rhythms - Definitions

General Terms:

Bradycardia - a heart rate that is lower than normal.

Tachycardia - a heart rate that is higher than normal.

Paroxysmal - an arrhythmia that suddenly begins and ends.

Specific Arrhythmias:

Sinus bradycardia - low sinus rate <60 beats="beats" br="br" min.="min.">
Sinus tachycardia - high sinus rate of 100-180 beats/min as occurs during exercise or other conditions that lead to increased SA nodal firing rate.

Sick sinus syndrome - a disturbance of SA nodal function that results in a markedly variable rhythm (cycles of bradycardia and tachycardia).

Atrial tachycardia - a series of 3 or more consecutive atrial premature beats occurring at a frequency >100/min; usually due to abnormal focus within the atria and paroxysmal in nature. This type of rhythm includes paroxysmal atrial tachycardia (PAT).

Atrial flutter - sinus rate of 250-350 beats/min.

Atrial fibrillation - uncoordinated atrial depolarizations.

Junctional escape rhythm - SA node suppression can result in AV node-generated rhythm of 40-60 beats/min (not preceded by p-wave).

AV nodal blocks - a conduction block within the AV node (or occasionally in the bundle of His) that impairs impulse conduction from the atria to the ventricles.

First-degree AV nodal block - the conduction velocity is slowed so that the P-R interval is increased to greater than 0.2 seconds. Can be caused by enhanced vagal tone, digitalis, beta-blockers, calcium channel blockers, or ischemic damage.

Second-degree AV nodal block - the conduction velocity is slowed to the point where some impulses from the atria cannot pass through the AV node. This can result in p-waves that are not followed by QRS complexes. For example, 1 or 2 p-waves may occur alone before one is followed by a QRS. When the QRS follows the p-wave, the P-R interval is increased. In this type of block, the ventricular rhythm will be less than the sinus rhythm.

Third-decree AV nodal block - conduction through the AV node is completely blocked so that no impulses are able to be transmitted from the atria to the ventricles. QRS complexes will still occur (escape rhythm), but they will originate from within the AV node, bundle of His, or other ventricular regions. Therefore, QRS complexes will not be preceded by p-waves. Furthermore, there will be complete asynchrony between the p-wave and QRS complexes. Atrial rhythm may be completely normal, but ventricular rhythm will be greatly reduced depending upon the location of the site generating the ventricular impulse. Ventricular rate typically range from 30 to 40 beats/min.

Supraventricular tachycardia (SVT) - usually caused by reentry currents within the atria or between ventricles and atria producing high heart rates of 140-250.

Ventricular premature beats (VPBs) - caused by ectopic ventricular foci; characterized by widened QRS.

Ventricular tachycardia (VT) - high ventricular rate caused by aberrant ventricular automaticity or by intraventricular reentry; can be sustained or non-sustained (paroxysmal); characterized by widened QRS; rates of 100 to 200 beats/min; life-threatening.

Ventricular flutter - ventricular depolarizations >200/min.

Ventricular fibrillation - uncoordinated ventricular depolarizations.