最も悲惨なタイプの心臓機能不全のいくつかは、心臓の不整脈が原因で発生します。たとえば、心房の拍動が心室の拍動と調和しなくなり、心房が心室充満を最適化する機能を果たせなくなることがあります。
この章の目的は、一般的な不整脈の生理学と心臓の拍動への影響、および心電図による診断について説明することです。不整脈の原因は通常、心臓の律動伝導系における以下の異常の 1 つまたは組み合わせです。
• Abnormal rhythmicity of the pacemaker
- Shift of the pacemaker from the sinus node to an- other place in the heart
- 心臓を通る刺激の伝播におけるさまざまなポイントでのブロック
- Abnormalpathwaysofimpulsetransmissionthrough the heart
- 心臓のほぼすべての部分で、偽の刺激が自然に発生する 異常な洞調律 頻脈頻脈という用語は、心拍数が速いことを意味し、成人では通常、100 回/分を超えると定義されます。頻脈の患者の心電図 (ECG) を図 13-1 に示します。この ECG は、QRS 群の時間間隔から決定される心拍数が、正常な 72 回/分ではなく約 150 回/分である点を除いて正常です。頻脈の原因には、体温の上昇、脱水、失血、貧血、交感神経による心臓の刺激、心臓の毒性状態などがあります。通常、体温が華氏 1 度上昇するごとに心拍数は 10 回/分ほど増加します (摂氏 1 度上昇するごとに 18 回/分増加)。体温が華氏 105 度 (摂氏 40.5 度) 程度まで上昇します。これを超えると、発熱による心筋の進行性衰弱のため、心拍数は減少することがあります。発熱により頻脈が生じるのは、体温の上昇により洞結節の代謝率が上昇し、その結果、洞結節の興奮性とリズム率が直接的に上昇するためです。
Many factors can cause the sympathetic nervous system to excite the heart, as discussed in this text. For example, when a patient sustains severe blood loss, sym- pathetic reflex stimulation of the heart may increase the heart rate to 150 to 180 beats/min. Simple weakening of the myocardium usually increases the heart rate because the weakened heart does not pump blood into the arte- rial tree to a normal extent, causing reductions in blood pressure and eliciting sympathetic reflexes to increase the heart rate.
BRADYCARDIA
The term bradycardia means a slow heart rate, usually defined as fewer than 60 beats/min. Bradycardia is shown by the ECG in Figure 13-2.
スポーツ選手の徐脈。よく訓練されたスポーツ選手の心臓は、普通の人よりも大きく、かなり強いことが多く、そのため、スポーツ選手の心臓は、休息中であっても、1 回の拍動で大きな拍出量を送り出すことができます。スポーツ選手が休息しているとき、拍動ごとに動脈樹に送り込まれる血液量が増えると、フィードバック循環反射または徐脈を引き起こすその他の影響が生じます。
迷走神経刺激は徐脈を引き起こします。迷走神経を刺激する循環反射はどれも、心臓の迷走神経終末でアセチルコリンを放出し、副交感神経効果をもたらします。おそらく、この現象の最も顕著な例は、頸動脈洞症候群の患者に発生します。これらの患者では、頸動脈壁の頸動脈洞領域にある圧力受容器（圧受容器）が過度に敏感です。そのため、首に軽い外部圧力がかかっただけでも、強い圧受容器反射が誘発され、極度の徐脈を含む、心臓に対する強い迷走神経アセチルコリン効果が生じます。この反射が強力すぎると、実際に心臓が 5 ～ 10 秒間停止し、意識喪失（失神）に至ることもあります。
SINUS ARRHYTHMIA
図 13-3 は、心拍数を心拍数計で記録したもので、最初は通常の呼吸中、記録の後半では深呼吸中である。心拍数計は、心電図における連続する QRS 群の間隔の持続時間を、連続するスパイクの高さで記録する機器である。この記録から、安静呼吸中 (記録の左半分に表示) の心拍数は 5% 以下しか増減していないことに注目する。その後、深呼吸中は、心拍数は呼吸サイクルごとに 30% も増減した。洞性不整脈は、心臓の洞結節への交感神経信号と副交感神経信号の強度を変える多くの循環器疾患のいずれかによって発生する可能性がある。呼吸性洞性不整脈は、主に呼吸の吸気と呼気のサイクル中に延髄呼吸中枢から隣接する血管運動中枢への信号の漏れによって生じます。漏れた信号により、交感神経と迷走神経を通じて心臓に伝達されるインパルスの数が交互に増加したり減少したりします。
心臓内伝導路における心ブロック
SINOATRIAL BLOCK
In rare cases, the impulse from the sinus node is blocked before it enters the atrial muscle. This phenomenon is demonstrated in Figure 13-4, which shows sudden ces- sation 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 atrioven- tricular (A-V) node, so the rate of the ventricular QRS-T complex is slowed but not otherwise altered. Sinoatrial block can be due to myocardial ischemia affecting the sinus node, inflammation or infection of the heart, or side effects from certain medications, and it can be observed in well-trained athletes.
ATRIOVENTRICULAR BLOCK
The only means whereby 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 of- ten delays or blocks conduction from the atria to the ventricles. Coronary insufficiency can cause is- chemia 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 ventri- cles. 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 cases 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 relationship to bradycardia.
5. Degeneration of the A-V conduction system, which is sometimes seen in older patients.
6. Medications such as digitalis or beta-adrenergic an- tagonists can, in some cases, impair A-V conduction.
INCOMPLETE ATRIOVENTRICULAR BLOCK
First-Degree Block—Prolonged P-R Interval. 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 more 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 13-5 shows an ECG with a prolonged P-R inter- val; the interval in this case is about 0.30 second instead of the normal 0.20 second 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 bun- dle is depressed so much that conduction stops entirely. One means for determining the severity of some heart diseases, such as acute rheumatic heart disease, for exam- ple, is to measure the P-R interval.
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 ven- tricles and sometimes not strong enough to do so. In this case, there will be an atrial P wave but no QRS-T wave, and it is said that there are “dropped beats” of the ven- tricles. This condition is called second-degree heart block.
There are two types of second-degree A-V block— Mobitz type I (also known as Wenckebach periodicity) and Mobitz type II. Type I block is characterized by progres- sive prolongation of the P-R interval until a ventricular beat is dropped and is then followed by resetting of the P-R interval 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 non- conducted 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. In contrast to type I block, with type II block the P-R interval does not change before the dropped beat; it remains fixed. 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 pro- gression to complete heart block and cardiac arrest.
Figure 13-6 shows progressive P-R interval prolonga- tion typical of type I (Wenckebach) block. Note prolon- gation of the P-R interval preceding the dropped beat, followed by a shortened P-R interval after the dropped beat.
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 im- pulse 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 dis- tal to the block. Therefore, the P waves become dissociated from the QRS-T complexes, as shown in Figure 13-7. Note that the rate of rhythm of the atria in this ECG is about 100 beats/min, whereas the rate of ventricular beat is less than 40 beats/min. Furthermore, there is no relationship 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 generat- ed distal to the A-V node or A-V bundle where the block occurs.
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, im- pulses 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 oc- curs 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/min, acting as the pacemaker of the ventricles. This phenom- enon 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/ min) usually pump enough blood to allow rapid recov- ery from the faint and then to sustain the person. These periodic fainting spells (syncope) 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 electri- cal 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 Pur- kinje system. Figure 13-8 shows the condition known as electrical alternans, which results from partial intraventricu- lar block every other heartbeat. This ECG also shows tachy- cardia (rapid heart rate), which is probably the reason the block has occurred. This is because when the rate of the heart is rapid, it may be impossible for some portions of the Pur- kinje system to recover from the previous refractory period quickly enough to respond during every succeeding heart- beat. Also, many conditions that depress the heart, such as ischemia, myocarditis, or digitalis toxicity, can cause incom- plete intraventricular block, resulting in electrical alternans.
PREMATURE CONTRACTIONS
A premature contraction is a contraction of the heart before the time that normal contraction would have been expected. This condition is also called extrasystole, pre- mature beat, or ectopic beat.
CAUSES OF PREMATURE CONTRACTIONS
Most premature contractions result from ectopic foci in the heart, which emit abnormal impulses at odd times during the cardiac rhythm. Possible causes of ectopic foci are as follows: (1) local areas of ischemia; (2) small calcified plaques at different points in the heart, which press against the adjacent cardiac muscle so that some of the fibers are irritated; and (3) toxic irritation of the A-V node, Purkinje system, or myocardium caused by infection, drugs, nicotine, or caffeine. The mechanical initiation of premature contractions is also frequent dur- ing cardiac catheterization; large numbers of premature contractions often occur when the catheter enters the ventricle and presses against the endocardium.
PREMATURE ATRIAL CONTRACTIONS
Figure 13-9 shows a single premature atrial contraction (PAC). The P wave of this beat occurred too soon in the heart cycle; the P-R interval is shortened, indicating that the ecto- pic origin of the beat is in the atria near the A-V node. Also, the interval between the premature contraction and the next succeeding contraction is slightly prolonged, which is called a compensatory pause. One of the reasons for this compensa- tory pause is that the premature contraction originated in the atrium some distance from the sinus node, and the impulse had to travel through a considerable amount of atrial muscle before it discharged the sinus node. Consequently, the sinus node discharged late in the premature cycle, which made the succeeding sinus node discharge also late in appearing.
PACs occur frequently in otherwise healthy people. They often occur in athletes whose hearts are in a very healthy condition. Mild toxic conditions resulting from such factors as smoking, lack of sleep, ingestion of too much coffee, alcoholism, and use of various drugs can also initiate such contractions.
Pulse Deficit. When the heart contracts ahead of sched- ule, the ventricles will not have filled with blood normally, and the stroke volume output during that contraction is depressed or is almost absent. Therefore, the pulse wave passing to the peripheral arteries after a premature con- traction may be so weak that it cannot be felt in the radial artery. Thus, a deficit in the number of radial pulses oc- curs when compared with the actual number of contrac- tions of the heart.
A-V NODAL OR A-V BUNDLE PREMATURE CONTRACTIONS
Figure 13-10 shows a premature contraction that origi- nated in the A-V node or A-V bundle. The P wave is missing from the electrocardiographic record of the pre- mature contraction. Instead, the P wave is superimposed onto the QRS-T complex because the cardiac impulse traveled backward into the atria at the same time that it traveled forward into the ventricles. This P wave slightly distorts the QRS-T complex, but the P wave itself can- not be discerned as such. In general, A-V nodal prema- ture contractions have the same significance and causes as atrial premature contractions.
PREMATURE VENTRICULAR CONTRACTIONS
The ECG in Figure 13-11 shows a series of premature ventricular contractions (PVCs) alternating with normal contractions in a pattern known as bigeminy. PVCs cause specific effects in the ECG, as follows:
1. The QRS complex is usually considerably prolonged. The reason for this prolongation is that the impulse is conducted mainly through slowly conducting muscle of the ventricles rather than through the Purkinje system.
2. The QRS complex has a high voltage. When the normal impulse passes through the heart, it pass- es through both ventricles nearly simultaneously. Consequently, in the normal heart, the depolariza- tion waves of the two sides of the heart—mainly of opposite polarity to each other—partially neutralize each other in the ECG. When a PVC occurs, the im- pulse almost always travels in only one direction, so there is no such neutralization effect, and one entire side or end of the ventricles is depolarized ahead of the other, which causes large electrical potentials, as shown for the PVCs in Figure 13-11.
3. After almost all PVCs, the T wave has an electrical potential polarity exactly opposite to that of the QRS complex because the slow conduction of the impulse through the cardiac muscle causes the muscle fibers that depolarize first also to repolarize first.
Some PVCs are relatively benign in their effects on overall pumping by the heart; they can result from such factors as cigarettes, excessive intake of coffee, lack of sleep, various mild toxic states, and even emotional irri- tability. Conversely, many other PVCs result from stray impulses or re-entrant signals that originate around the borders of infarcted or ischemic areas of the heart. The presence of such PVCs is not to be taken lightly. People with significant numbers of PVCs often have a much higher than normal risk of developing spontaneous lethal ventricular fibrillation, presumably initiated by one of the PVCs. This development is especially true when the PVCs occur during the vulnerable period for causing fibrillation, just at the end of the T wave, when the ventricles are com- ing out of refractoriness, as explained later in this chapter.
Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction. In Chapter 12, the principles of vectorial analysis are explained. By applying these princi- ples, one can determine from the ECG in Figure 13-11 the point of origin of the PVC, as follows. Note that the potentials of the premature contractions in leads II and III are both strongly positive. On plotting these potentials on the axes of leads II and III and solving by vectorial analy- sis for the mean QRS vector in the heart, one finds that the vector of this premature contraction has its negative end (origin) at the base of the heart and its positive end toward the apex. Thus, the first portion of the heart to become depolarized during this premature contraction is near the base of the ventricles, which therefore is the ori- gin of the ectopic focus.
Disorders of Cardiac Repolarization—the Long QT Syndromes. Recall that the Q wave corresponds to ven- tricular depolarization, whereas the T wave corresponds to ventricular repolarization. The Q-T interval is the time from the Q point to the end of the T wave. Disorders that delay repolarization of ventricular muscle after the action potential cause prolonged ventricular action potentials and therefore excessively long Q-T intervals on the ECG, a condition called long QT syndrome (LQTS).
The major reason that LQTS is of concern is that delayed repolarization of ventricular muscle increases a person’s susceptibility to developing ventricular arrhyth- mias called torsades de pointes, which literally means “twisting of the points.” This type of arrhythmia has the features shown in Figure 13-12. The shape of the QRS complex may change over time, with the onset of arrhyth- mia usually following a premature beat, a pause, and then another beat with a long Q-T interval, which may trigger arrhythmias, tachycardia and, in some cases, ventricular fibrillation.
Disorders of cardiac repolarization that lead to LQTS may be inherited or acquired. The congenital forms of LQTS are rare disorders caused by mutations of sodium or potassium channel genes. At least 17 different muta- tions of these genes causing variable degrees of Q-T pro- longation have been identified.
More common are the acquired forms of LQTS that are associated with plasma electrolyte disturbances, such as hypomagnesemia, hypokalemia, or hypocalcemia, or with the administration of excess amounts of antiarrhyth- mic drugs such as quinidine or some antibiotics such as fluoroquinolones or erythromycin, which prolong the Q-T interval.
Although some people with LQTS exhibit no major symptoms (other than the prolonged Q-T interval), other people exhibit fainting and experience ventricular arrhythmias that may be precipitated by physical exercise, intense emotions such as fright or anger, or being startled by a noise. The ventricular arrhythmias associated with LQTS can, in some cases, deteriorate into ventricular fibrillation and sudden death.
Treatment may include magnesium sulfate for acute LQTS and antiarrhythmic medications such as beta- adrenergic blockers or surgical implantation of a cardiac defibrillator for long-term LQTS.
PAROXYSMAL TACHYCARDIA
Some abnormalities in different portions of the heart, including the atria, Purkinje system, or ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart. This phenomenon is believed to be caused most frequently by re-entrant circus movement feedback pathways that set up local repeated self–re-excitation. Because of the rapid rhythm in the irritable focus, this focus becomes the pace- maker of the heart.
The term paroxysmal means that the heart rate becomes rapid in paroxysms, with the paroxysm begin- ning suddenly and lasting for a few seconds, a few min- utes, a few hours, or much longer. The paroxysm usually ends as suddenly as it began, with the pacemaker of the heart instantly shifting back to the sinus node.
Paroxysmal tachycardia often can be stopped by elicit- ing a vagal reflex. A type of vagal reflex sometimes elicited for this purpose is to press on the neck in the regions of the carotid sinuses, which may cause enough of a vagal reflex to stop the paroxysm. Antiarrhythmic drugs may also be used to slow conduction or prolong the refractory period in cardiac tissues.
PAROXYSMAL ATRIAL TACHYCARDIA
Figure 13-13 demonstrates a sudden increase in the heart rate from about 95 to about 150 beats/min in the middle of the record. On close study of the ECG, an inverted P wave is seen during the rapid heartbeat before each QRS-T complex, and this P wave is partially super- imposed onto the normal T wave of the preceding beat. This finding indicates that the origin of this paroxysmal tachycardia is in the atrium but, because the P wave is abnormal in shape, the origin is not near the sinus node.
A-V Nodal Paroxysmal Tachycardia. Paroxysmal tachy- cardia often results from an aberrant rhythm involving the A-V node that usually causes almost normal QRS-T complexes but totally missing or obscured P waves.
Atrial or A-V nodal paroxysmal tachycardia, both of which are referred to as supraventricular tachycardias, usually occur in young, otherwise healthy people, and they generally grow out of the predisposition to tachycar- dia after adolescence. In general, supraventricular tachy- cardia frightens a person tremendously and may cause weakness during the paroxysm, but it usually does not cause permanent harm from the attack.
VENTRICULAR TACHYCARDIA
Figure 13-14 shows a typical short paroxysm of ventricu- lar tachycardia. The ECG of ventricular tachycardia has the appearance of a series of ventricular premature beats occurring one after another, without any normal beats interspersed.
Ventricular tachycardia is usually a serious condition for two reasons. First, this type of tachycardia usually does not occur unless considerable ischemic damage is present in the ventricles. Second, ventricular tachycar- dia frequently initiates the lethal condition of ventricular fibrillation because of rapid repeated stimulation of the ventricular muscle, as discussed in the next section.
Sometimes, intoxication from the heart failure treat- ment drug digitalis causes irritable foci that lead to ventricular tachycardia. Antiarrhythmic drugs such as amiodarone or lidocaine can be used to treat ventricular tachycardia. Lidocaine depresses the normal increase in sodium permeability of the cardiac muscle membrane during generation of the action potential, thereby often blocking the rhythmical discharge of the focal point that has been causing the paroxysmal attack. Amiodarone has multiple actions, such as prolonging the action potential and refractory period in cardiac muscle and slowing A-V conduction. In some cases, cardioversion with an electric
shock to the heart is needed for restoration of normal heart rhythm.
VENTRICULAR FIBRILLATION
The most serious of all cardiac arrhythmias is ventricular fibrillation, which, if not stopped within 1 to 3 minutes, is almost invariably fatal. Ventricular fibrillation results from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating first one portion of the ventricular muscle, then another portion, then another, and eventually feeding back onto itself to re- excite the same ventricular muscle over and over, never stopping. When this phenomenon occurs, many small portions of the ventricular muscle will be contracting at the same time, while equally as many other portions will be relaxing. Thus, there is never a coordinated contraction of all the ventricular muscle at once, which is required for a pumping cycle of the heart. Despite massive movement of stimulatory signals throughout the ventricles, the ven- tricular chambers neither enlarge nor contract but remain in an indeterminate stage of partial contraction, pumping either no blood or negligible amounts. Therefore, after fibrillation begins, unconsciousness occurs within 4 to 5 seconds because of lack of blood flow to the brain, and irretrievable death of tissues begins to occur throughout the body within a few minutes.
Multiple factors can spark the beginning of ventricu- lar fibrillation; a person may have a normal heartbeat one moment, but 1 second later, the ventricles are in fibril- lation. Especially likely to initiate fibrillation are sudden electrical shock of the heart, ischemia of the heart muscle, or ischemia of the specialized conducting system.
PHENOMENON OF RE-ENTRY—CIRCUS MOVEMENTS AS THE BASIS FOR VENTRICULAR FIBRILLATION
When the normal cardiac impulse in the normal heart has traveled through the extent of the ventricles, it has no place to go because all the ventricular muscle is refractory and cannot conduct the impulse farther. Therefore, that impulse dies, and the heart awaits a new action potential to begin in the sinus node.
Under some circumstances, however, this normal sequence of events does not occur. Therefore, the follow- ing is a more complete explanation of the background conditions that can initiate re-entry and lead to what is referred to as circus movements, which in turn cause ven- tricular fibrillation.
Figure 13-15 shows several small cardiac muscle strips cut in the form of circles. If such a strip is stimulated at the 12 o’clock position so that the impulse travels in only one direction, the impulse spreads progressively around the circle until it returns to the 12 o’clock position. If the originally stimulated muscle fibers are still in a refractory state, the impulse then dies out because refractory muscle cannot transmit a second impulse. However, three dif- ferent conditions can cause this impulse to continue to travel around the circle—that is, cause re-entry of the impulse into muscle that has already been excited (circus movement):
- If the pathway around the circle is much longer than normal, by the time the impulse returns to the 12 o’clock position, the originally stimulated muscle will no longer be refractory, and the impulse will continue around the circle again and again.
- If the length of the pathway remains constant but the velocity of conduction becomes decreased enough, an increased interval of time will elapse be- fore the impulse returns to the 12 o’clock position. By this time, the originally stimulated muscle might be out of the refractory state, and the impulse can continue around the circle again and again.
- The refractory period of the muscle might become greatly shortened. In this case, the impulse could also continue around and around the circle.
All these conditions occur in different pathological states of the human heart: (1) a long pathway typically occurs in dilated hearts; (2) a decreased rate of conduc- tion frequently results from blockage of the Purkinje sys- tem, ischemia of the muscle, high blood potassium levels, or many other factors; and (3) a shortened refractory period commonly occurs in response to various drugs, such as epinephrine, or after repetitive electrical stimu- lation. Thus, in many cardiac disturbances, re-entry can cause abnormal patterns of cardiac contraction or abnor- mal cardiac rhythms that ignore the pace-setting effects of the sinus node.
CHAIN REACTION MECHANISM OF FIBRILLATION
In ventricular fibrillation, one sees many separate and small contractile waves spreading at the same time in dif- ferent directions over the cardiac muscle. The re-entrant impulses in fibrillation are not simply a single impulse moving in a circle, as shown in Figure 13-15. Instead, they have degenerated into a series of multiple wave fronts that have the appearance of a chain reaction. One of the best ways to explain this process in fibrillation is to describe the initiation of fibrillation by electric shock with a 60-cycle alternating electric current.
Fibrillation Caused by 60-Cycle Alternating Current.
At a central point in the ventricles of heart A in Figure 13-16, a 60-cycle electrical stimulus is applied through a stimulating electrode. The first cycle of the electrical stimulus causes a depolarization wave to spread in all directions, leaving all the muscle beneath the electrode in a refractory state. After about 0.25 second, part of this muscle begins to come out of the refractory state. Some portions come out of refractoriness before other portions. This state of events is depicted in heart A by many lighter patches, which represent excitable cardiac muscle, and dark patches, which represent muscle that is still refractory. Now, continuing 60-cycle stimuli from the electrode can cause impulses to travel only in certain di- rections through the heart but not in all directions. Thus, in heart A, certain impulses travel for short distances un- til they reach refractory areas of the heart, and then they are blocked. However, other impulses pass between the refractory areas and continue to travel in the excitable areas. Then, several events transpire in rapid succession, all occurring simultaneously and eventuating in a state of fibrillation.
First, block of the impulses in some directions but suc- cessful transmission in other directions creates one of the necessary conditions for a re-entrant signal to develop— that is, transmission of some of the depolarization waves around the heart in only some directions but not in other directions.
Second, the rapid stimulation of the heart causes two changes in the cardiac muscle, both of which predispose to circus movement: (1) the velocity of conduction through the heart muscle decreases, which allows a longer time interval for the impulses to travel around the heart; and (2) the refractory period of the muscle is shortened, allow- ing re-entry of the impulse into previously excited heart muscle within a much shorter time than normal.
Third, one of the most important features of ventricu- lar fibrillation is the division of impulses, as demonstrated in heart A in Figure 13-16. When a depolarization wave reaches a refractory area in the heart, it travels to both sides around the refractory area. Thus, a single impulse becomes two impulses. Then, when each of these impulses reaches another refractory area, it divides to form two more impulses. In this way, many new wave fronts are continually being formed in the heart by pro- gressive chain reactions until, finally, many small depolar- ization waves are traveling in many directions at the same time. Furthermore, this irregular pattern of impulse travel causes many circuitous routes for the impulses to travel, greatly lengthening the conductive pathway, which is one of the conditions that sustains the fibrillation. It also results in a continual irregular pattern of patchy refractory areas in the heart.
One can readily see when a vicious circle has been initi- ated. More and more impulses are formed; these impulses cause more and more patches of refractory muscle, and the refractory patches cause more and more division of the impulses. Therefore, whenever a single area of cardiac muscle comes out of refractoriness, an impulse is close at hand to re-enter the area.
Heart B in Figure 13-16 demonstrates the final state that develops in ventricular fibrillation. Here, one can see many impulses traveling in all directions, with some divid- ing and increasing the number of impulses and others blocked by refractory areas. A single electric shock during this vulnerable period frequently can lead to an odd pattern of impulses spreading multidirectionally around refractory areas of muscle, which will lead to ventricular fibrillation.
ELECTROCARDIOGRAM IN VENTRICULAR FIBRILLATION
In ventricular fibrillation, the ECG is bizarre (Figure 13-17) and ordinarily shows no tendency toward a regu- lar rhythm of any type. During the first few seconds of ventricular fibrillation, relatively large masses of muscle contract simultaneously, which causes coarse irregular waves in the ECG. After another few seconds, the coarse contractions of the ventricles disappear, and the ECG changes into a new pattern of low-voltage, very irregular waves. Thus, no repetitive electrocardiographic pattern can be ascribed to ventricular fibrillation. Instead, the
ventricular muscle contracts at as many as 30 to 50 small patches of muscle at a time, and electrocardiographic potentials change constantly and spasmodically because the electrical currents in the heart flow first in one direc- tion and then in another and seldom repeat any specific cycle.
The voltages of the waves in the ECG in ventricular fibrillation are usually about 0.5 millivolt when ventricular fibrillation first begins, but they decay rapidly; thus, after 20 to 30 seconds, they are usually only 0.2 to 0.3 millivolt. Minute voltages of 0.1 millivolt or less may be recorded for 10 minutes or longer after ventricular fibrillation begins. As already noted, because no pumping of blood occurs during ventricular fibrillation, this state is lethal unless stopped by successful therapy, such as an imme- diate electroshock (defibrillation) through the heart, as explained in the next section.
VENTRICULAR DEFIBRILLATION
Although a moderate alternating current voltage applied directly to the ventricles almost invariably throws the ven- tricles into fibrillation, a strong high-voltage electrical cur- rent passed through the ventricles for a fraction of a second can stop fibrillation by throwing all the ventricular muscle into refractoriness simultaneously. This is accomplished by passing intense current through large electrodes placed on two sides of the heart. The current penetrates most of the fibers of the ventricles at the same time, thus stimulating essentially all parts of the ventricles simultaneously and causing them all to become refractory. All action potentials stop, and the heart remains quiescent for 3 to 5 seconds, after which it begins to beat again, usually with the sinus node or some other part of the heart becoming the pace- maker. However, if the same re-entrant focus that had orig- inally thrown the ventricles into fibrillation is still present, fibrillation may begin again immediately.
When electrodes are applied directly to the two sides of the heart, fibrillation can usually be stopped using 1000 volts of direct current applied for a few thousandths of a second. When applied through two electrodes on the chest wall, as shown in Figure 13-18, the usual procedure is to charge a large electrical capacitor up to several thou- sand volts and then to cause the capacitor to discharge for a few thousandths of a second through the electrodes and through the heart.
In most cases, defibrillation current is delivered to the heart in biphasic waveforms, alternating the direction of the current pulse through the heart. This form of deliv- ery substantially reduces the energy needed for successful defibrillation, thereby decreasing the risk for burns and cardiac damage.
In patients with a high risk for ventricular fibrillation, a small, battery-powered, implantable cardioverter- defibrillator (ICD) with electrode wires lodged in the right ventricle may be implanted. The device is pro- grammed to detect ventricular fibrillation and revert it by delivering a brief electrical impulse to the heart. Advances in electronics and batteries have permitted the development of ICDs that can deliver enough electrical current to defibrillate the heart through electrode wires implanted subcutaneously, outside the rib cage near the heart rather than in or on the heart itself. These devices can be implanted with a minor surgical procedure.
HAND PUMPING OF THE HEART (CARDIOPULMONARY RESUSCITATION) AS AN AID TO DEFIBRILLATION
Unless defibrillated within 1 minute after ventricular fibrillation begins, the heart is usually too weak to be revived by defibrillation because of the lack of nutrition from coronary blood flow. However, it is still possible to revive the heart by preliminarily pumping the heart by hand (intermittent hand squeezing) and then defibrillat- ing the heart later. In this way, small quantities of blood are delivered into the aorta, and a renewed coronary blood supply develops. Then, after a few minutes of hand pumping, electrical defibrillation often becomes possible. Fibrillating hearts have been pumped by hand for as long as 90 minutes followed by successful defibrillation.
A technique for pumping the heart without opening the chest consists of intermittent thrusts of pressure on the chest wall along with artificial respiration. This process, plus defi- brillation, is called cardiopulmonary resuscitation (CPR).
Lack of blood flow to the brain for more than 5 to 8 minutes usually causes permanent mental impairment or even destruction of brain tissue. Even if the heart is revived, the person may die from the effects of brain dam- age or may live with permanent mental impairment.
ATRIAL FIBRILLATION
Remember that except for the conducting pathway through the A-V bundle, the atrial muscle mass is sepa- rated from the ventricular muscle mass by fibrous tissue. Therefore, ventricular fibrillation often occurs without atrial fibrillation. Likewise, fibrillation often occurs in the atria without ventricular fibrillation (shown on the right in Figure 13-20).
The mechanism of atrial fibrillation is identical to that of ventricular fibrillation, except that the process occurs only in the atrial muscle mass instead of the ventricu- lar mass. A frequent cause of atrial fibrillation is atrial enlargement, which can result, for example, from heart valve lesions that prevent the atria from emptying ade- quately into the ventricles or from ventricular failure with excess damming of blood in the atria. The dilated atrial walls provide ideal conditions of a long conductive path- way, as well as slow conduction, both of which predispose to atrial fibrillation.
Impaired Pumping of the Atria During Atrial Fibril- lation. For the same reasons that the ventricles will not pump blood during ventricular fibrillation, neither do the atria pump blood in atrial fibrillation. Therefore, the atria become useless as primer pumps for the ventricles. Even so, blood flows passively through the atria into the ven- tricles, and the efficiency of ventricular pumping is de- creased by only 20% to 30%. Therefore, in contrast to the lethality of ventricular fibrillation, a person can live for years with atrial fibrillation, although at reduced efficien- cy of overall heart pumping. However, due to the reduced atrial contractile function, blood can stagnate, allowing blood clots to form in the atrial appendage. These blood clots can dislodge and travel to the brain, causing stroke, or to other parts of the body. Therefore, patients with atrial fibrillation are often placed on blood thinner medi- cations (anticoagulants) to reduce the risk of embolism.
ELECTROCARDIOGRAM IN ATRIAL FIBRILLATION
Figure 13-19 shows the ECG during atrial fibrillation. Numerous small depolarization waves spread in all directions through the atria during atrial fibrillation. Because the waves are weak, and many of them are of opposite polarity at any given time, they usually almost completely electrically neu- tralize one another. Therefore, in the ECG, one can see either no P waves from the atria or only a fine, high-frequency, very
low voltage wave record. Conversely, the QRS-T complexes are normal unless there is some pathology of the ventricles, but their timing is irregular, as explained next.
IRREGULARITY OF VENTRICULAR RHYTHM DURING ATRIAL FIBRILLATION
When the atria are fibrillating, impulses arrive from the atrial muscle at the A-V node rapidly but also irregularly. Because the A-V node will not pass a second impulse for about 0.35 second after a previous one, at least 0.35 second must elapse between one ventricular contraction and the next. Then, an additional but variable interval of 0 to 0.6 second occurs before one of the irregular atrial fibrillatory impulses happens to arrive at the A-V node. Thus, the interval between successive ventricular contrac- tions varies from a minimum of about 0.35 second to a maximum of about 0.95 second, causing a very irregular heartbeat. In fact, this irregularity, demonstrated by the variable spacing of the heartbeats in the ECG shown in Figure 13-19, is one of the clinical findings used to diag- nose the condition. Also, because of the rapid rate of the fibrillatory impulses in the atria, the ventricle is driven at a fast heart rate, usually between 125 and 150 beats/min.
ELECTROSHOCK TREATMENT OF ATRIAL FIBRILLATION
Similar to ventricular fibrillation being converted back to a normal rhythm by electroshock, so can atrial fibrillation be converted by electroshock. The procedure is similar as that for ventricular fibrillation conversion, except the single electric shock is programmed (or synchronized) to fire only during the QRS complex when the ventricles are refractory to stimulation. A normal rhythm often follows if the heart is capable of generating a normal rhythm. This procedure is called synchronized cardioversion instead of defibrillation in the setting of ventricular fibrillation.
ATRIAL FLUTTER
Atrial flutter is another condition caused by a circus movement in the atria. Atrial flutter is different from atrial fibrillation in that the electrical signal travels as a single large wave, always in one direction, around and around the atrial muscle mass, as shown to the left in Figure 13-20. Atrial flutter causes a rapid rate of contraction of the atria, usually between 200 and 350 beats/min. How- ever, because one side of the atria is contracting while the other side is relaxing, the amount of blood pumped by the atria is reduced. Furthermore, the signals reach the A-V node too rapidly for all of them to be passed into the ven- tricles because the refractory periods of the A-V node and A-V bundle are too long to pass more than a fraction of the atrial signals. Therefore, there are usually two to three beats of the atria for every single beat of the ventricles.
Figure 13-21 shows a typical ECG in atrial flutter. The P waves are strong because of the contraction of semico- ordinated masses of muscle. However, note that a QRS-T complex follows an atrial P wave only once for every two beats of the atria, giving a 2:1 rhythm.
CARDIAC ARREST
A final serious abnormality of the cardiac rhythmicity- conduction system is cardiac arrest, which results from cessation of all electrical control signals in the heart. That is, no spontaneous rhythm remains.
Cardiac arrest may occur during deep anesthesia, when severe hypoxia may develop because of inadequate respiration. The hypoxia prevents the muscle fibers and conductive fibers from maintaining normal electrolyte concentration differentials across their membranes, and their excitability may be so affected that the automatic rhythmicity disappears.
In many cases of cardiac arrest from anesthesia, pro- longed CPR (for many minutes or even hours) is quite successful in re-establishing a normal heart rhythm. In some patients, severe myocardial disease can cause per- manent or semipermanent cardiac arrest, which can cause death. To treat the condition, rhythmical electrical impulses from an implanted electronic cardiac pacemaker have been used successfully to keep patients alive for months to years.
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