Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 19. Cardiac Arrest and Sudden Cardiac Death

The preceding chapters systematically discussed the major disorders of heart rhythm and atrioventricular (AV) conduction. Instead of considering entirely new ECG patterns, this chapter reviews some earlier topics, placing them in a special clinical perspective. The subject of this chapter is the 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.


The patient in cardiac arrest loses consciousness within seconds and may even have a seizure as a result of inadequate blood flow to the brain. Irreversible brain damage usually occurs within 4 minutes and sometimes sooner. Furthermore, shortly after the heart stops pumping, spontaneous breathing also ceases (cardiopulmonary arrest). Respiration sometimes stops first (primary respiratory arrest) and cardiac activity stops shortly thereafter.

The diagnosis of cardiac arrest should be made clinically even before the patient is connected to an ECG machine. Laypeople should immediately recognize cardiac arrest in any unresponsive person who is not breathing. Trained clinicians should examine the patient very quickly by trying to feel for pulses in the carotid arteries. The patient in cardiac arrest becomes cyanotic (bluish gray) from lack of oxygenated blood. No heart tones are audible with a stethoscope placed on the chest, and the blood pressure is, of course, unobtainable. The arms and legs become cool. If the brain becomes severely hypoxic, the pupils are fixed and dilated. Seizure activity may occur. However, the absence of pulses in an unresponsive individual is the major diagnostic sign of cardiac arrest.

When cardiac arrest is recognized, cardiopulmonary resuscitation (CPR) must be started without delay. In capsule form, the initial basic life support treatment of any cardiac arrest consists of the following four (A, B, C, D) steps:



Establish an Airway.



Breathe for the patient, either by mouth-to-mouth or mouth-to-mask methods or by manually compressing a bag-valve device, forcing air into the patient's nose or mouth.



Maintain Circulation by external cardiac compression.



Defibrillate the heart.

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.

Initial treatment with ventilation and external cardiac compression should never be delayed while the patient in cardiac arrest is being connected to an ECG recorder.



The three basic ECG patterns seen with cardiac arrest were mentioned in earlier chapters. Cardiac arrest may be associated with the following:



Ventricular tachyarrhythmia, including ventricular fibrillation (VF) or a sustained type of pulseless ventricular tachycardia (VT)



Ventricular asystole or a brady-asystolic rhythm with an extremely slow rate



Pulseless electrical activity (PEA), also referred to as electromechanical dissociation (EMD)

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 [1] [2] [3] [4] [5] [6]).

FIGURE 19-1  Ventricular fibrillation causing cardiac arrest.

FIGURE 19-2  Ventricular tachycardia (VT) and ventricular fibrillation (VF) recorded during cardiac arrest (monitor leads). The rapid sine-wave type of ventricular tachycardia seen here is sometimes referred to as ventricular flutter.

FIGURE 19-3  Complete ventricular standstill (asystole) producing a straight-line pattern during cardiac arrest.

FIGURE 19-4  Escape rhythms with underlying ventricular standstill (monitor leads). A, Junctional escape rhythm with narrow QRS complexes. B, Idioventricular escape rhythm with wide QRS complexes. Treatment should include the use of intravenous atropine and, if needed, sympathomimetic drugs in an attempt to speed up these bradycardias, which cannot support the circulation. If hyperkalemia is present, it should be treated.

FIGURE 19-5  External cardiac compression artifact. External cardiac compression during resuscitation produces artifactual ECG complexes (C), which may be mistaken for QRS complexes.

FIGURE 19-6  ECG “history” of cardiac arrest and successful resuscitation. The left panel shows the ECG sequence during an actual cardiac arrest. The right panel shows sequential therapy used in this case for the different ECG patterns. A and B, Initially, the ECG showed ventricular asystole with a straight-line pattern, which was treated by external cardiac compression, along with intravenous medications. Intravenous vasopressin may also be used here. C and D, Next ventricular fibrillation was seen. Intravenous amiodarone and other medications may also be used in this setting (see text and references). E to G, Sinus rhythm appeared after defibrillation with a direct-current electric shock. C, external cardiac compression artifact; DC, direct current; R, R wave from the spontaneous QRS complex; V, ventricular premature beat.


With 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 .

Of the three basic ECG patterns seen with cardiac arrest, VF is the most common one encountered initially. It may appear spontaneously, although as noted in Chapter 16 , it often is preceded by another ventricular arrhythmia (usually 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, with a defibrillator (cardioverter) used to administer a direct-current electric shock to the heart by means of paddles placed on the chest wall. An example of successful defibrillation is presented in Figure 19-6 D.

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

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

In cases where VF or pulseless VT persists or recurs despite initial defibrillation attempts, additional measures are indicated, including drugs to support the circulation (epinephrine or vasopressin), intravenous antiarrhythmic agents such as amiodarone or lidocaine, and magnesium sulfate (if hypomagnesemia is suspected).


Ventricular standstill and slow escape rhythms are described in Chapter 13 . 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, AV junction, or ventricles) takes over. In such cases, the ECG records a straight-line pattern (seeFig. 19-3 ), indicating asystole. Whenever you encounter a straight-line pattern, you need to confirm this finding in at least two leads 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 may also mimic a straight-line pattern.

The treatment of ventricular standstill also requires continued external cardiac compression. 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, which may be inserted at the bedside in an emergency situation. As described in Chapter 21 , the temporary transvenous pacemaker is a special catheter wire electrode that is usually inserted through a vein into the right ventricle and connected to a battery outside the body. A type of external temporary pacemaker that does not require intravenous insertion is also commercially available. This noninvasive (transcutaneous) pacemaker uses special electrodes that are pasted on the chest wall. Transcutaneous pacing may not always be effective, however, and it can be quite painful in conscious patients.

Hyperkalemia should always be excluded in cases of brady-asystolic rhythms.

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 beat (see Chapter 13 ). 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. 19-4 A). In others, they come from a lower focus in the ventricles, producing a slowidioventricular rhythm with wide QRS complexes (see Fig. 19-4 B). The term brady-asystolic pattern is used to describe this type of cardiac arrest ECG.

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).


In the large majority of patients with cardiac arrest, the ECG shows either a sustained ventricular tachyarrhythmia (VF or VT) or a brady-asystolic pattern. Occasionally, however, the ECG of patients in cardiac arrest surprisingly continues to show identifiable, narrow QRS complexes at a relatively physiologic rate. The actual heart rhythm in such cases may be a sinus rhythm, AV junctional (nodal) rhythm, AF, or other supraventricular mechanism. Despite the presence of recurring QRS complexes and even P waves on the ECG, however, the patient is unconscious and does not have a palpable pulse or blood pressure detectable by usual clinical methods. In other words, the patient has cardiac electrical activity but insufficient mechanical heart contractions to pump blood effectively. The termpulseless electrical activity (PEA) or electromechanical dissociation (EMD) is used in such cases.

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. These include severe hypovolemia, hypoxemia,and acidosis. Another important reversible cause of EMD is pericardial (cardiac) tamponade, in which pericardial effusion decreases cardiac output and ultimately causes cardiac arrest. Pericardial tamponade can be treated by removing some of the fluid from the pericardial sac with a special needle inserted through the chest wall (pericardiocentesis). Because the disease process is primarily extracardiac (i.e., involving the pericardium), the ECG generally shows relatively normal electrical activity, despite the impaired mechanical function of the heart. Low voltage with sinus tachycardia is often present. Electrical alternans may be seen (see Chapter 11 ). Tension pneumothorax and massive pulmonary embolism are two other potentially reversible causes of EMD ( Table 19-1 ).

TABLE 19-1   -- Some Conditions That Cause Pulseless Electrical Activity




History of blood or fluid loss, flat neck veins


Cyanosis, abnormal blood gases, airway problems

Cardiac (pericardial) tamponade

History of trauma, renal failure, or thoracic malignancy; no pulse with cardiopulmonary resuscitation, neck vein distension, impending tamponade (tachycardia, hypotension, low pulse pressure) changing to sudden bradycardia as the terminal event

Tension pneumothorax

History of asthma, ventilator use, chronic obstructive pulmonary disease, or trauma; no pulse with cardiopulmonary resuscitation, absent breath sounds, neck vein distension, tracheal deviation


History of exposure to cold; low central body temperature

Massive pulmonary embolism

Relevant history, no pulse felt with cardiopulmonary resuscitation, distended neck veins

Drug overdose (tricyclic antidepressants, digoxin, beta blockers, calcium channel blockers)

Bradycardia, history of drug ingestion, empty medication bottles at the scene, neurologic examination


ECG showing wide QRS complexes without P waves and then asystole; history of renal failure, diabetes, dialysis, or selected medications

Severe acidosis

History of preexisting acidosis, renal failure, diabetes mellitus

Acute, massive myocardial infarction

Relevant history, ECG, cardiac enzymes

Modified from Cummins RO (ed): Textbook of Advanced Cardiac Life Support, Dallas, TX, American Heart Association, 1997.


One of the most common settings in which EMD 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 three basic ECG patterns seen with cardiac arrest are a sustained ventricular tachyarrhythmia, ventricular asystole (or brady-asystolic patterns), and pulseless electrical activity. 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.



Cardiac arrest associated with any of the three electrical mechanisms—ventricular tachyarrhythmia, ventricular asystole, or PEA—may occur in numerous settings. It can be due to any type of organic heart disease. For example, a patient with an acute MI may have cardiac arrest for several reasons. Myocardial ischemia and increased ventricular electrical instability may precipitate VF. Damage to the conduction system may result in ventricular standstill. Finally, EMD may occur with extensive myocardial injury. Occasionally, actual rupture of the infarcted ventricular wall occurs, leading to fatal pericardial tamponade. Cardiac arrest also occurs when electrical instability is associated with chronic heart disease resulting from previous infarction, valvular abnormalities, hypertension, or cardiomyopathy.

A lightning strike or an electric shock 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 drugs may lead to torsades de pointes (see Chapter 16 ). Excessive digitalis can also lead to fatal ventricular arrhythmias (see Chapter 18 ). Hypokalemia and hypomagnesemia may potentiate arrhythmias associated with a variety of antiarrhythmic drugs and with digitalis glycosides. Other cardiac drugs can also precipitate sustained ventricular tachyarrhythmias through their so-called proarrhythmic effects (see Chapter 16 ). The recreational use of cocaine may also induce fatal arrhythmias.

Brady-asystolic cardiac arrest may occur with intrinsic conduction disease resulting from sick sinus syndrome (see Chapters 13 and 20 ) or with high-degree AV block (see Chapter 17 ). You need to exclude very important reversible causes of brady-asystolic arrest such as hyperkalemia (see Chapter 10 ) and drug toxicity (e.g., digitalis, tricyclic antidepressant overdose, beta blockers, calcium channel blockers). Systemic hypothermia may be associated with severe bradycardia. Conditions that may directly cause or contribute to pulseless electrical activity (including brady-asystolic patterns or actual EMD) are summarized in Table 19-1 .

During and after successful resuscitation of the patient in cardiac arrest, an intensive search for the cause 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 pertinent medical history should be obtained from every available source, with particular attention to drug use (e.g., digitalis, antiarrhythmics, psychotropics, “recreational” drugs) and previous cardiac problems.



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. More than 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 bradyasystolic mechanism or EMD.

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 sudden cardiac death have structural heart disease with valvular abnormalities or myocardial disease associated, for example, with severe aortic stenosis, dilated or hypertrophic cardiomyopathy, acute or chronic myocarditis, arrhythmogenic right ventricular dysplasia, or anomalous origin of a coronary artery.

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 precipitating ventricular fibrillation), the Brugada syndrome, or severe SA or AV conduction system disease causing prolonged sinus arrest or high grade heart block, respectively.

QT prolongation, a marker of risk for torsades de pointes type of ventricular tachycardia, was discussed in Chapters 10 and 16 . QT prolongation syndromes may be divided into acquired and hereditary (congenital) subsets. The major acquired causes include drugs, electrolyte abnormalities, and bradyarrhythmias. 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 clinical factors causing long QT is given in Chapter 24 .

FIGURE 19-7  Patient on quinidine (monitor lead) developed marked prolongation of repolarization with low amplitude T-U waves (A) followed by cardiac arrest with torsades de pointes ventricular tachycardia (B). (Note that the third beat in panel A is a premature atrial complex.)

FIGURE 19-8  Hereditary long QT syndrome. ECG from 21-year-old woman with history of recurrent syncope, initially mistaken for a seizure disorder. The ECG demonstrates a prolonged QT interval of 0.6 second. Note the broad T waves with notching (or possibly U waves) in the precordial leads. Syncope, with risk of sudden cardiac death, is due to episodes of torsades de pointes type of ventricular tachycardia.

The Brugada syndrome refers to the association of a characteristic ECG pattern with risk of ventricular tachyarrhythmias. The Brugada pattern consists of distinctive ST elevations in the right chest leads (V1 to 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.

FIGURE 19-9  Brugada pattern showing characteristic ST elevations in the right chest leads. The ECG superficially resembles a right bundle branch block (RBBB) pattern. Typical RBBB, however, produces an rSR′ pattern in right precordial leads and is not associated with ST elevation in this distribution. The Brugada pattern appears to be a marker of abnormal right ventricular repolarization and in some individuals is associated with an increased risk of life-threatening ventricular arrhythmias.

As noted, “recreational” drugs such as cocaine or cardiac antiarrhythmic agents may induce lethal arrhythmias. Finally, a small subset of individuals sustain cardiac arrest without having any demonstrable structural or currently identifiable electrophysiologic abnormality.

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 ventricular fibrillation. This syndrome has been most frequently reported after chest wall impact during sports such as baseball or softball, football or rugby, boxing, ice hockey, karate, and lacrosse, but may occur in other settings, 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 .



Cardiac arrest occurs when the heart stops pumping blood. The diagnosis should be made clinically even before the patient is connected to an electrocardiograph. The major clinical sign of cardiac arrest is the absence of pulses in an unconscious patient.

Cardiac arrest may be associated with one or more of the following ECG patterns:



Ventricular tachyarrhythmias, including ventricular fibrillation, sustained typical ventricular tachycardia, torsades de pointes, or ventricular flutter



Ventricular standstill (asystole) or bradyasystolic pattern, which is a straight-line pattern, sometimes with interruptions by junctional or ventricular escape beats



Pulseless electrical activity (PEA)/Electromechanical dissociation (EMD), in which recurring QRS complexes and sometimes even P waves are not associated with a palpable pulse or blood pressure. EMD is usually caused by diffuse myocardial injury, although it may be due to pericardial tamponade, tension pneumothorax, or massive pulmonary embolism, among other causes.

Any or all of these patterns may be seen during the resuscitation of a patient in cardiac arrest.

With cardiac arrest, the ECG may show distinctive artifacts caused by external cardiac compression. These large wide deflections should not be mistaken for the intrinsic electrical activity of the heart.

The term sudden cardiac death is used in reference to individuals who sustain an unexpected cardiac arrest and, unless resuscitated, die instantly or within an hour or so of the development of acute symptoms.





Would a pacemaker be of any value in treating a patient with cardiac arrest and electromechanical dissociation (EMD)?



The rhythm strip shown below was obtained from a patient during the course of a cardiac arrest and attempted resuscitation. Answer the following questions:




What is the basic rhythm?



What is the likely cause of the complexes marked X?



Name four drugs that can produce cardiac arrest associated with a sustained ventricular tachyarrhythmia (i.e., ventricular fibrillation, monomorphic ventricular tachycardia, torsades de pointes, or ventricular flutter).