Contraction
Atrioventricular Node
+++++++++++
Conduction through the AV node is slow, requiring about 0.15 seconds. (This delay provides time for atrial contraction to propel blood into the ventricles.) The impulse then propagates down the His-Purkinje system and invades all parts of the ventricles, beginning with the endocardial surface near the apex and ending with the epicardial surface at the base of the heart. Activation of the entire ventricular myocardium is complete in less than 0.1 second. As a result, ventricular contraction is synchronous and hemodynamically effective. Arrhythmias represent electrical activity that deviates from the above description as a result of an abnormality in impulse initiation and/or impulse propagation.
Next, the impulse stimulates specialized conduction tissues in the atrioventricular (AV) nodal and His-bundle areas; together, these two regions constitute the AV junction. The bundle of His fans bifurcates into two main branches, the right and left bundles, which rapidly transmit depolarization wavefronts in a synchronous way to the right and left ventricular myocardium by way of Purkinje fibers. The main left bundle bifurcates into left anterior and left posterior fascicle subdivisions. The depolarization wavefronts then spread through the ventricular wall, from endocardium to epicardium, triggering coordinated ventricular contraction. Since the cardiac depolarization and repolarization waves have directions and magnitudes, they can be represented by vectors.
The AV node acts to delay the impulses by approximately 120ms, to ensure the atria have enough time to fully eject blood into the ventricles before ventricular systole.
The wave of excitation then passes from the atrioventricular node into the atrioventricular bundle.
The AV node’s primary function is to delay electrical conduction from the atria to the ventricles, allowing for sequential and coordinated atrial and ventricular mechanical contraction.
The compact AV node (~1 × 3 × 5 mm) is situated at the apex of the triangle of Koch, which is defined by the coronary sinus ostium posteriorly, the septal tricuspid valve annulus anteriorly, and the tendon of Todaro superiorly.
The AV node, which is located in the septal wall of the right atrium, just anterior to the opening of the coronary sinus and above the insertion of the septal leaflet of the tricuspid valve, is actually made up of three distinct areas: an upper junctional (AN) region, a middle nodal (N) region, and a lower junctional (NH) region. Although the N region does not possess intrinsic spontaneous activity (automaticity), both junctional areas do.
The compact AV node continues as the penetrating AV bundle where it immediately traverses the central fibrous body and is in close proximity to the aortic, mitral, and tricuspid valve annuli;
The normally slower rate of spontaneous depolarization in AV junctional areas (40-60 times/min) allows the faster SA node to control heart rate. Any factor that decreases the rate of SA node depolarization or increases the automaticity of AV junctional areas allows the junctional areas to function as the pacemaker for the heart. Impulses from the SA node normally reach the AV node after about 0.04 sec, but leave after another 0.11 sec. This delay is the result of the slowly conducting small myocardial fibers within the AV node, which depend on slow calcium channels for propagation of the action potential. In contrast, conduction of the impulse between adjoining cells in the atria and in the ventricles is due primarily to activation of sodium channels.
The AV node is under direct influence of the parasympathetic and sympathetic nervous system; parasympathetic input decreases conduction speed in the AV node and increases refractoriness, and sympathetic input increases conduction speed and shortens refractoriness. In contrast, normal conduction in the His bundle is not significantly influenced by the autonomic nervous system.
The lower fibers of the AV node combine to form the common bundle of His.
> NEXT: 05. His and Purkinje Fibers
+++++++++++++++++++++
"| EKG Correlation | |
|---|---|
|
A. Sinus p waves are characterized by a frontal plane axis directed inferiorly and leftward, with positive p waves in leads II, III, and aVF; an initially positive biphasic p wave in V1and a negative p wave in aVR . Sinus tachycardia (>100 beats/min) typically occurs in response to sympathetic stimulation and vagal withdrawal, whereby the rate of spontaneous depolarization of the sinus node increases and the focus of earliest activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to normal sinus rhythm. B. Right atrial anatomy seen from a right lateral perspective with the lateral wall opened to view the septum. AVN, atrioventricular node; CS Os, coronary sinus ostium; FO, fossa ovalis; IVC, inferior vena cava; SVC, superior vena cava; TVA, tricuspid valve annulus. |
Potent inhaled anesthetics depress SA node automaticity. These agents seem to have only modest direct effects on the AV node, prolonging conduction time and increasing refractoriness. This combination of effects likely explains the occurrence of junctional tachycardia when an anticholinergic is administered for sinus bradycardia during inhalation anesthesia; junctional pacemakers are accelerated more than those in the SA node. The electrophysiological effects of volatile agents on Purkinje fibers and ventricular muscle are complex due to autonomic interactions. Both antiarrhythmic and arrhythmogenic properties are described. The former may be due to direct depression of Ca2+ influxes, whereas the latter generally involves potentiation of catecholamines, especially with
halothane. The arrhythmogenic effect requires activation of both α1- and β-adrenergic receptors. Intravenous induction agents have limited electrophysiological effects in usual clinical doses. Opioids, particularly
fentanyl and
sufentanil, can depress cardiac conduction, increasing AV node conduction and the refractory period and prolonging the duration of the Purkinje fiber action potential.
Local anesthetics have important electrophysiological effects on the heart at blood concentrations that are generally associated with systemic toxicity. In the case of lidocaine, electrophysiological effects at low blood concentrations can be therapeutic. At high blood concentrations, local anesthetics depress conduction by binding to sodium channels; at extremely high concentrations, they also depress the SA node. The most potent local anesthetics—bupivacaine, etidocaine, and to a lesser degree, ropivacaine—seem to have the most potent effects on the heart, particularly on Purkinje fibers and ventricular muscle. Bupivacaine binds open or inactivated sodium channels and dissociates from them slowly. It can cause profound sinus bradycardia and sinus node arrest and malignant ventricular arrhythmias; furthermore, it can depress left ventricular contractility. Twenty percent lipid emulsions have been used to treat local anesthetic cardiac toxicity. The mechanisms of action of this therapy are unclear, although possibilities include serving as a lipid reservoir and decreasing lipophilic toxic local anesthetics in the myocardium.
Calcium channel blockers are organic compounds that block Ca2+ influx through L-type but not T-type channels. Dihydropyridine blockers, such as nifedipine, simply plug the channel, whereas other agents, such as verapamil, and to a lesser extent, diltiazem, preferentially bind the channel in its depolarized inactivated state (use-dependent blockade).
Most produce narrow QRS-complex tachycardia (QRS duration <120 ms) characteristic of ventricular activation over an unblocked Purkinje system. Conduction block in the left or right bundle branch or activation of the ventricles from an accessory pathway produces a wide QRS complex
Clinical Correlation Study Question
An 87-year-old man with a history of well-treated hypertension and aortic stenosis has become symptomatic from his aortic stenosis over the last 2 months. Yesterday, he underwent surgical aortic valve replacement with a bioprosthetic 25-mm valve with excellent intraoperative results. He was rapidly weaned from cardiopulmonary bypass and extubated within 24 hours. Per surgical protocol, he had temporary epicardial pacing wires placed on the ventricular surface and has been pacing at 90 bpm. On rounds this morning, you briefly pause his ventricular pacing to check his underlying rhythm. You note an atrial rate of 80 bpm, but a ventricular rate of 32 bpm with a wide QRS complex. There is no relationship between the P waves and QRS complexes. This patient’s ventricular bradycardia is most likely due to which of the following?
The answer is E. The compact AV node (~1 × 3 × 5 mm) is situated at the apex of the triangle of Koch, which is defined by the coronary sinus ostium posteriorly, the septal tricuspid valve annulus anteriorly, and the tendon of Todaro superiorly. The compact AV node continues as the penetrating AV bundle where it immediately traverses the central fibrous body and is in close proximity to the aortic, mitral, and tricuspid valve annuli; thus, it is subject to injury in the setting of valvular heart disease or its surgical treatment. It is common for patients to experience transient AV block after valve surgery (particularly aortic valve surgery) due to the surrounding edema. Many patients will regain normal conduction as the perioperative injury and edema decrease; however, some patients will not and will require permanent pacemaker placement. It is unlikely that this patient has developed new systemic disease such as Lyme disease, sarcoidosis, or endocarditis. SA nodal disease would manifest as sinus bradycardia, which this patient does not have.