Sudden Cardiac Arrest and Sudden Cardiac Death

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Chapter 19 Sudden Cardiac Arrest and Sudden Cardiac Death

Please go to expertconsult.com for supplemental chapter material.

The subject of this chapter is the ECG recognition of life-threatening arrhythmias that cause cardiac arrest. By definition, cardiac arrest occurs when the heart stops contracting effectively and ceases to pump blood. The important and closely related topic of sudden cardiac death is also introduced.

Clinical Aspects of Cardiac Arrest

The patient in cardiac arrest loses consciousness within seconds, and irreversible brain damage usually occurs within 4 minutes, sometimes sooner. Furthermore, shortly after the heart stops pumping, spontaneous breathing also ceases (cardiopulmonary arrest). In some cases, respirations stop first (primary respiratory arrest) and cardiac activity stops shortly thereafter.

No heart tones are audible with a stethoscope placed on the chest, and the blood pressure is unobtainable. The patient in cardiac arrest becomes cyanotic (bluish gray) from lack of circulating oxygenated blood, and the arms and legs become cool. If the brain becomes severely hypoxic, the pupils are fixed and dilated. Seizure activity may occur.

When cardiac arrest is recognized, cardiopulmonary resuscitation (CPR) efforts must be started without delay. The latest (2010) recommendations for the general public in the initial basic life support treatment of a witnessed cardiac arrest involve an approach of effective, continuous chest compressions without interruption for mouth-to-mouth resuscitation (so-called hands-only resuscitation). These new recommendations (Box 19-1) are designed to improve the practice of resuscitation in untrained bystanders; they apply to adults, children, and infants but exclude newborns.

The guidelines do recognize that, in some circumstances, conventional CPR (with a 30:2 compression-to-breath ratio) may provide more benefit than hands-only CPR. Some examples of these circumstances include the following:

The specific details of CPR and advanced cardiac life support including intubation, drug dosages, the use of automatic emergency defibrillators (AEDs) and standard defibrillators, along with other matters related to definitive diagnosis and treatment, lie outside the scope of this book but are discussed in selected references cited in the Bibliography. This chapter concentrates on the particular ECG patterns seen during cardiac arrest and the clinical implications of these major abnormalities.

Basic ECG Patterns in Cardiac Arrest

The three basic ECG patterns seen with cardiac arrest were mentioned in earlier chapters. Cardiac arrest may be associated with the ECG patterns listed in Box 19-2.

The ECG patterns seen in cardiac arrest are briefly reviewed in the following sections, with emphasis placed on their clinical implications (Figs. 19-1 to 19-6).

Ventricular Tachyarrhythmia (Ventricular Fibrillation or Pulseless VT)

With ventricular fibrillation (VF) the ventricles do not contract but instead twitch rapidly in a completely ineffective way. No cardiac output occurs, and the patient loses consciousness within seconds. The characteristic ECG pattern, with its unmistakable fast oscillatory waves, is illustrated in Figure 19-1.

VF may appear spontaneously, as noted in Chapter 14, but is often preceded by another ventricular arrhythmia (usually ventricular tachycardia [VT] or premature ventricular beats). Figure 19-2 shows a run of VT degenerating into VF during cardiac arrest.

The treatment of VF was described in Chapter 16. The patient should be immediately defibrillated, given a direct current electric shock (360 joules) to the heart by means of paddles or pads placed on the chest wall (usually in an anterior-posterior position).

VT and VF are the only “shockable” sudden cardiac arrest rhythms. An example of successful defibrillation is presented in Figure 19-6D.

Success in defibrillating any patient depends on a number of factors. The single most important factor in treating VF is haste: the less delay in defibrillation, the greater the chance of succeeding.

Sometimes repeated shocks must be administered before the patient is successfully resuscitated. In other cases, all attempts fail. Finally, external cardiac compression must be continued between attempts at defibrillation.

In addition to defibrillation, additional measures include intravenous drugs to support the circulation (epinephrine or vasopressin) and antiarrhythmic agents such as amiodarone or lidocaine, and magnesium sulfate (in cases of torsades de pointes and when hypomagnesemia is present).

Ventricular Asystole and Brady-Asystolic Rhythms

The normal pacemaker of the heart is the sinus node, which is located in the right atrium. Failure of the sinus node to function (sinus arrest) leads to ventricular standstill (asystole) if no other subsidiary pacemaker (e.g., in the atria, atrioventricular [AV] junction, or ventricles) takes over. In such cases the ECG records a straight-line pattern (see Fig. 19-3), indicating asystole. Whenever you encounter a straight-line pattern, you need to confirm this finding in at least two leads (as seen in most conventional telemetry systems) and check to see that all electrodes are connected to the patient. Electrodes often become disconnected during a cardiac arrest, leading to the mistaken diagnosis of asystole. Very low amplitude VF (so-called “fine VF”) may also mimic a straight-line pattern. Increasing the gain on the monitor may reveal this “hidden” VF pattern.

The treatment of asystole also requires continued external cardiac compression; however, unlike VT or VF, defibrillation is not appropriate, nor effective. Sometimes spontaneous cardiac electrical activity resumes. Drugs such as vasopressin or epinephrine may help support the circulation or stimulate cardiac electrical activity. Patients with refractory ventricular standstill require a temporary pacemaker, inserted into the right ventricle through the internal jugular or femoral veins. Noninvasive, transcutaneous pacing uses special electrodes that are pasted on the chest wall. However, transcutaneous pacing may only be effective with bradycardia, not frank asystole, and it may be quite painful in conscious patients.

Not uncommonly with ventricular standstill, you also see occasional QRS complexes appearing at infrequent intervals against the background of the basic straight-line rhythm. These are escape beats and represent the attempt of intrinsic cardiac pacemakers to restart the heart’s beating (see Chapter 14). Examples of escape rhythms with underlying ventricular standstill are shown in Figure 19-4. In some cases the escape beats are narrow, indicating their origin from either the atria or the AV junction (see Fig. 19-4A). In others they come from a lower focus in the ventricles, producing a slow idioventricular rhythm with wide QRS complexes (see Fig. 19-4B). The term brady-asystolic pattern is used to describe this type of cardiac arrest ECG.

Hyperkalemia, as well as other potentially reversible causes, such as drugs or ischemia, should always be excluded in cases of brady-asystolic rhythms.

Escape beats should not be confused with artifacts produced by external cardiac compression. Artifacts are large, wide deflections that occur with each compression (see Fig. 19-5). Their size varies with the strength of the compression, and their direction varies with the lead in which they appear (i.e., usually negative in leads II, III, and aVF, positive in leads aVR and aVL).

Pulseless Electrical Activity (Electromechanical Dissociation)

In occasional patients with cardiac arrest, the person is unconscious and does not have a palpable pulse or blood pressure despite the presence of recurring QRS complexes and even P waves on the ECG. In other words, the patient has cardiac electrical activity but insufficient mechanical heart contractions to pump blood effectively. This syndrome is called pulseless electrical activity (PEA) or electromechanical dissociation (EMD). Similar to asystole, defibrillation is not appropriate therapy for PEA.

PEA with a physiologic rate can arise in a number of settings. When assessing a patient with PEA, you must consider potentially reversible causes first. Box 19-3 presents an adaptation of the classic “5 Hs and the 5 Ts” that may lead to PEA.

One of the most common settings in which PEA occurs is when the myocardium has sustained severe generalized injury that may not be reversible, such as with myocardial infarction (MI). In such cases, even though the heart’s conduction system may be intact enough to generate a relatively normal rhythm, the amount of functional ventricular muscle is insufficient to respond to this electrical signal with an adequate contraction. Sometimes the myocardial depression is temporary and reversible (“stunned myocardium”), and the patient may respond to resuscitative efforts.

In summary, the main ECG patterns seen with cardiac arrest are a sustained ventricular tachyarrhythmia or VF, ventricular asystole (including brady-asystolic patterns), and PEA. During the course of resuscitating any patient, you may see two or even all three of these ECG patterns at different times during the arrest. Figure 19-6 shows the “ECG history” of a cardiac arrest.

Clinical Causes of Cardiac Arrest

Cardiac arrest may occur in numerous settings. It can be due to any type of organic heart disease. For example, a patient with an acute or prior MI (Box 19-4) may have cardiac arrest for at least five reasons.

Cardiac arrest may also occur when severe electrical instability is associated with other types of chronic heart disease resulting from valvular abnormalities, hypertension, or cardiomyopathy.

An electric shock (including a lightning strike) may produce cardiac arrest in the normal heart. Cardiac arrest may also occur during surgical procedures, particularly in patients with underlying heart disease.

Drugs such as epinephrine can produce VF. Quinidine, disopyramide, procainamide, ibutilide, dofetilide, and related “antiarrhythmic” drugs may lead to long QT(U) syndrome with torsades de pointes (see Chapter 16). Digitalis toxicity can also lead to fatal ventricular arrhythmias (see Chapter 18). Other cardiac drugs may also precipitate sustained ventricular tachyarrhythmias through their so-called proarrhythmic effects (see Chapter 16). The recreational use of cocaine may also induce fatal arrhythmias.

Hypokalemia and hypomagnesemia may potentiate arrhythmias associated with a variety of antiarrhythmic drugs and with digitalis glycosides.

During and after successful resuscitation of the patient in cardiac arrest, an intensive search for the cause(s) must be started. Serial 12-lead ECGs and serum cardiac enzyme levels are helpful in diagnosing MI. A complete blood count, serum electrolyte concentrations, and arterial blood gas measurements should be obtained. A portable chest x-ray unit and, if needed, an echocardiograph machine can be brought to the bedside. In addition, a careful physical examination (signs of congestive heart failure, pneumothorax, etc.) should be performed in concert with a pertinent medical history with particular attention to drug use (e.g., digitalis, antiarrhythmics, psychotropics, “recreational” drugs, etc.) and previous cardiac problems.

Sudden Cardiac Death/Arrest

The term sudden cardiac death is used to describe the situation in which an individual who sustains an unexpected cardiac arrest and is not resuscitated dies instantly or within an hour or so of the development of acute symptoms. Over 400,000 such deaths occur each year in the United States, striking individuals both with and without known cardiovascular disease. Unexpected sudden cardiac death is most often initiated by a sustained ventricular tachyarrhythmia, less commonly by a brady-asystolic mechanism or PEA.

Most individuals with unexpected cardiac arrest have underlying structural heart disease. An estimated 20% of patients with acute MI die suddenly before reaching the hospital. Another important substrate for sudden death is severe left ventricular scarring from previous (chronic) MI.

Other patients with unexpected sudden cardiac arrest have structural heart disease with valvular abnormalities or myocardial disease associated, for example, with severe aortic stenosis, dilated or hypertrophic cardiomyopathy, myocarditis, arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), or anomalous origin of a coronary artery.

QT prolongation, a marker of risk for torsades de pointes type of VT, was discussed in Chapter 17. QT prolongation syndromes may be divided into acquired and hereditary (congenital) subsets. The major acquired causes include drugs, electrolyte abnormalities, and bradyarrhythmias, especially high-degree AV blocks. Figure 19-7 shows an example of marked QT prolongation due to quinidine that was followed by torsades de pointes and cardiac arrest. Hereditary long QT syndromes (Fig. 19-8) are due to a number of different abnormalities of cardiac ion channel function (“channelopathies”). A detailed list of factors causing long QT syndrome and risk of torsades is given in Chapter 24.

Some individuals with sudden cardiac death do not have mechanical cardiac dysfunction, but they may have intrinsic electrical instability as a result of the long QT syndromes (predisposing to torsades de pointes), Wolff-Parkinson-White (WPW) preexcitation syndrome (particularly when associated with atrial fibrillation with a very rapid ventricular response precipitating VF), the Brugada syndrome, and severe sinoatrial (SA) or AV conduction system disease causing prolonged sinus arrest or high-grade heart block, respectively.

The Brugada syndrome refers to the association of a characteristic ECG pattern with risk of ventricular tachyarrhythmias. The Brugada pattern consists of unusual ST segment elevations in the right chest leads (V1-V3) with a QRS pattern somewhat resembling a right bundle branch block (Fig. 19-9). The basis of the Brugada pattern and associated arrhythmias is a topic of active study. Abnormal repolarization of right ventricular muscle related to sodium channel dysfunction appears to play an important role.

A rare cause of recurrent syncope and sometimes sudden cardiac arrest and death is catecholaminergic polymorphic ventricular tachycardia (CPVT), typically induced by exercise or stress. Some cases are familial (autosomal dominant) related to a genetic mutation that alters calcium dynamics in myocytes.

Another rare but reported cause of cardiac arrest from ventricular tachyarrhythmias (and sometimes atrial fibrillation) in young individuals is the so-called “short QT syndrome.” As implied by the name these individuals usually have an ECG showing an abbreviated ST segment and a very short QTc (usually <330 msec). This abnormal repolarization (the opposite of long QT in its appearance) is likely due to abnormal function of one or more cardiac ion channels. However, the link between very short QT in certain individuals and ventricular arrhythmogenesis remains unresolved.

As noted, “recreational” drugs, such as cocaine, or cardiac antiarrhythmic agents, such as flecainide and quinidine, may induce lethal arrhythmias. A small subset of individuals sustains sudden cardiac arrest without having any demonstrable structural or currently identifiable electrophysiologic abnormality.

Finally, the term commotio cordis (Latin for “cardiac concussion”) refers to the syndrome of sudden cardiac arrest in healthy individuals who sustain nonpenetrating chest trauma triggering VF. This syndrome has been most frequently reported after chest wall impact during sports, but may occur during other activities, such as car or motorcycle accidents.

The identification and management of patients at high risk for sudden death are central areas of investigation in cardiology today. The important role of implantable cardioverter-defibrillator (ICD) devices in preventing sudden death in carefully selected high-risk patients is discussed in Chapter 21.