In rare instances, the impulse from the sinus node is blocked before it enters the atrial muscle. This phenomenon is demonstrated in Figure 1, which shows sudden cessation of P waves, with resultant standstill of the atria. However, the ventricles pick up a new rhythm, with the impulse usually originating spontaneously in the atrioventricular (A-V) node, so the rate of the ventricular QRS-T complex is slowed but not otherwise altered.

Fig1. Sinoatrial (SA) nodal block, with atrioventricular nodal  rhythm during the block period (lead III). 

ATRIOVENTRICULAR BLOCK

 The only means by which impulses ordinarily can pass from the atria into the ventricles is through the A-V bundle, also known as the bundle of His. Conditions that can either decrease the rate of impulse conduction in this bundle or block the impulse entirely are as follows:

1. Ischemia of the A-V node or A-V bundle fibers often delays or blocks conduction from the atria to the ventricles. Coronary insufficiency can cause ischemia of the A-V node and bundle in the same way that it can cause ischemia of the myocardium.

 2. Compression of the A-V bundle by scar tissue or by calcified portions of the heart can depress or block conduction from the atria to the ventricles.

3. Inflammation of the A-V node or A-V bundle can depress conduction from the atria to the ventricles. Inflammation results frequently from different types of myocarditis that are caused, for example, by diphtheria or rheumatic fever.

4. Extreme stimulation of the heart by the vagus nerves in rare instances blocks impulse conduction through the A-V node. Such vagal excitation occasionally results from strong stimulation of the baroreceptors in people with carotid sinus syndrome, discussed earlier in relation to bradycardia.

INCOMPLETE ATRIOVENTRICULAR HEART BLOCK

Prolonged P-R (or P-Q) Interval—First-Degree Block. The usual lapse of time between the beginning of the P wave and the beginning of the QRS complex is about 0.16 second when the heart is beating at a normal rate. This so-called P-R interval usually decreases in length with a faster heartbeat and increases with a slower heartbeat. In general, when the P-R interval increases to greater than 0.20 second, the P-R interval is said to be prolonged and the patient is said to have first-degree incomplete heart block.

Figure 2 shows an ECG with a prolonged P-R interval; the interval in this instance is about 0.30 second instead of the normal 0.20 or less. Thus, first-degree block is defined as a delay of conduction from the atria to the ventricles but not actual blockage of conduction. The P-R interval seldom increases above 0.35 to 0.45 second because, by that time, conduction through the A-V bundle is depressed so much that conduction stops entirely. One means for determining the severity of some heart dis eases, such as acute rheumatic heart disease, for example, is to measure the P-R interval.

Fig2. Prolonged P-R interval caused by first-degree atrioventricular heart block (lead II).

Second-Degree Block. When conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second, the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not strong enough to do so. In this instance, there will be an atrial P wave but no QRS-T wave, and it is said that there are “dropped beats” of the ventricles. This condition is called second-degree heart block. 

There are two types of second-degree A-V block: type I (also known as Wenckebach periodicity) and type II. Type I block is characterized by progressive prolongation of the PR interval until a ventricular beat is dropped and is then followed by resetting of the PR and repeating of the abnormal cycle. A type I block is almost always caused by abnormality of the A-V node. In most cases, this type of block is benign and no specific treatment is needed.

In type II block there is usually a fixed number of nonconducted P waves for every QRS complex. For example, a 2 : 1 block implies that there are two P waves for every QRS complex. At other times, rhythms of 3 : 2 or 3 : 1 may develop. Type II block is generally caused by an abnormality of the bundle of His-Purkinje system and may require implantation of a pacemaker to prevent progression to complete heart block and cardiac arrest.

Figure 3 shows P-R intervals of 0.30 second, as well as one dropped ventricular beat as a result of failure of conduction from the atria to the ventricles.

Fig3. Second-degree atrioventricular block, showing occasional failure of the ventricles to receive the excitatory signals (lead  V3). 

Complete A-V Block (Third-Degree Block). When the condition causing poor conduction in the A-V node or A-V bundle becomes severe, complete block of the impulse from the atria into the ventricles occurs. In this case, the ventricles spontaneously establish their own signal, usually originating in the A-V node or A-V bundle distal to the block. Therefore, the P waves become dis sociated from the QRS-T complexes, as shown in Figure4. Note that the rate of rhythm of the atria in this ECG is about 100 beats per minute, whereas the rate of ventricular beat is less than 40 per minute. Furthermore, there is no relation between the rhythm of the P waves and that of the QRS-T complexes because the ventricles have “escaped” from control by the atria and are beating at their own natural rate, controlled most often by rhythmical signals generated distal to the A-V node or A-V bundle where the block occurs.

Fig4. Complete atrioventricular block (lead II). 

Stokes-Adams Syndrome—Ventricular Escape. In some patients with A-V block, the total block comes and goes; that is, impulses are conducted from the atria into the ventricles for a period of time and then suddenly impulses are not conducted. The duration of block may be a few seconds, a few minutes, a few hours, or even weeks or longer before conduction returns. This condition occurs in hearts with borderline ischemia of the conductive system.

Each time A-V conduction ceases, the ventricles often do not start their own beating until after a delay of 5 to 30 seconds. This delay results from the phenomenon called overdrive suppression. Overdrive suppression means that ventricular excitability is at first suppressed because the ventricles have been driven by the atria at a rate greater than their natural rate of rhythm. However, after a few seconds, some part of the Purkinje system beyond the block, usually in the distal part of the A-V node beyond the blocked point in the node, or in the A-V bundle, begins discharging rhythmically at a rate of 15 to 40 times per minute and acting as the pacemaker of the ventricles. This phenomenon is called ventricular escape.

Because the brain cannot remain active for more than 4 to 7 seconds without blood supply, most people faint a few seconds after complete block occurs because the heart does not pump any blood for 5 to 30 seconds, until the ventricles “escape.” After escape, however, the slowly beating ventricles (typically beating less than 40 beats per minute) usually pump enough blood to allow rapid recovery from the faint and then to sustain the person. These periodic fainting spells are known as the Stokes-Adams syndrome.

Occasionally the interval of ventricular standstill at the onset of complete block is so long that it becomes detrimental to the patient’s health or even causes death. Consequently, most of these patients are provided with an artificial pacemaker, a small battery-operated electrical stimulator planted beneath the skin, with electrodes usually connected to the right ventricle. The pacemaker provides continued rhythmical impulses to the ventricles.

INCOMPLETE INTRAVENTRICULAR BLOCK—ELECTRICAL ALTERNANS

Most of the same factors that can cause A-V block can also block impulse conduction in the peripheral ventricular Purkinje system. Figure 5 shows the condition known as electrical alternans, which results from partial intraventricular block every other heartbeat. This ECG also shows tachycardia (rapid heart rate), which is prob ably the reason the block has occurred, because when the rate of the heart is rapid, it may be impossible for some portions of the Purkinje system to recover from the previous refractory period quickly enough to respond during every succeeding heartbeat. Also, many conditions that depress the heart, such as ischemia, myocarditis, or digitalis toxicity, can cause incomplete intraventricular block, resulting in electrical alternans.

Fig5.  Partial intraventricular block—“electrical alternans”  (lead II). 

اخر الاخبار

اخبار العتبة العباسية المقدسة

أكاديمية التطوير الإداري تنظّم دورة في اللغة الفارسية لعدد من ملاكات العتبة العباسية المقدسة

استعدادًا لافتتاحه.. المشرف على قسم الشؤون الطبية يجري جولة في مركز السيد جعفر الحلي للخدمات الطبية.

الهيأة العليا لإحياء التراث تقيم الدورة العلمية التخصصية لكتاب في رحاب العقيدة

سماحة السيد الصافي يؤكد ضرورة تنمية الموارد المالية لدائرة التقاعد الوطنية وتعظيمها

المزيد

الآخبار الصحية

العلاج بالماء البارد.. باحثون يكشفون فوائده الصحية

من دون صالة رياضية.. عادة بسيطة لتحسين الصحة وخسارة الوزن

لصحة القلب وتفادي السرطان.. استهلك هذا النوع من الطعام

دراسة تحذر من خطر شرب القهوة في أكواب البلاستيك

المزيد

الآخبار التكنلوجية

إنجاز طبي تاريخي.. جراحة قلب بلا شق في الصدر

اليابان.. مراحيض توفر فحص للحالة الصحية عبر "تحليل البراز" !

اختراق واسع لمنصة "إنستغرام".. ونشر بيانات على "الدارك ويب"

علماء يحذرون: هكذا سيفنى كوكب الأرض

المزيد

مواضيع ذات صلة

Basic Principles of Circulatory Function

Physical Characteristics of the Circulation

Abnormal Sinus Rhythms Tachycardia

Flow of Current Around the Heart During the Cardiac Cycle

Voltage and Time Calibration of The Electrocardiogram

Characteristics of the Normal Electrocardiogram: Depolarization Waves versus Repolarization Waves

Control of Excitation and Conduction in The Heart

Automatic Electrical Rhythmicity of the Sinus Fibers

Regulation of Heart Pumping

Diastole and Systole

ACTION POTENTIALS IN CARDIAC MUSCLE

Fibrinolysis