Even in communities that have effective programs for prehospital cardiac care, only a fraction of cardiac arrest patients will survive to hospital admission. The immediate goal for rescuers in the field is restoration of spontaneous circulation. If that can be achieved, preservation of the brain, heart, and other vital organs must be considered. Potential complications of the resuscitation must be identified and treatment instituted. The probable cause, including reversible precipitating events, the nature and severity of any underlying heart disease, and the arrhythmia probably responsible for the episode, should be determined. Finally, therapy can be selected and its potential for success evaluated.
Complications of Resuscitation
Only a fraction of cardiac arrest survivors who receive early defibrillation will be alert and oriented with full recovery of function at the time of hospital admission. Most patients will have pulmonary, cardiac, or neurologic complications resulting from the period of arrest or the resuscitation itself. Pulmonary complications are usually due either to aspiration of gastric contents or to mechanical injury to the thoracic cage during closed-chest compressions. The chest wall should be carefully inspected, palpated, and stabilized, if necessary. In extreme cases, bony thoracic fractures may result in a flail chest, or hepatic or splenic lacerations may occur. Chest radiography may be helpful in detecting aspiration, but repeated examinations may be necessary to document the delayed appearance of infiltrates. If a central line has been placed, the chest radiograph is also useful to confirm catheter position and to exclude a pneumothorax. Mechanical ventilation is often required in the early period after admission to allow adequate oxygenation and pulmonary cleansing; this may require the use of muscle relaxants and sedation. Over oxygenation should be avoided.
Early revascularization should be attempted in all cardiac arrest survivors who present with a new ST segment elevation myocardial infarction and should be considered whenever acute ischemia was a likely contributor to the arrest. Some cardiac arrest centers have urged that all cardiac arrest survivors undergo coronary angiography immediately after resuscitation, but this may not be possible in all hospitals. If an acute total coronary occlusion is identified, revascularization is indicated.
Cardiac arrest even without a new coronary occlusion produces a period of global cardiac ischemia, frequently resulting in a period of cardiac stunning, defined as a reversible depression in cardiac systolic function. Inotropic or even mechanical (eg, intra-aortic balloon counterpulsation) support may be necessary to maintain vital organ perfusion during the early phase after resuscitation. Any acute assessment of ventricular function may overestimate the amount of permanent dysfunction, and a low ejection fraction measured in the first several days after arrest may not be an accurate gauge of eventual cardiac function. Arrhythmias are frequently seen during the period immediately after resuscitation. They may be similar to those that originally produced the arrest, or they may be new rhythm disturbances caused by poor hemodynamic function and multiorgan failure. No single therapy will be predictably effective against these arrhythmias, and antiarrhythmic agents, β-adrenergic blockers, positive inotropic agents, and other measures to improve hemodynamic function must be tried. Recent studies using intravenous amiodarone prior to hospital admission have demonstrated improvements in rates of return of spontaneous circulation and survival-to-hospital admission but no clear benefit in survival-to-hospital discharge.
If spontaneous circulation can be restored and the patient is admitted to the hospital, neurologic damage is the major cause of death and long-term disability. Neurologic damage occurs quickly during a cardiac arrest. Unless defibrillation with restoration of spontaneous circulation was almost immediate, patients will be unconscious when admitted to the hospital, and an accurate evaluation of the potential for functional recovery is often difficult in this early stage. Brainstem reflexes may be preserved, but their presence does not necessarily predict a favorable outcome. Generalized or focal seizure activity, decerebrate or decorticate posturing, and involuntary respiratory efforts may make mechanical ventilation difficult. Neuromuscular blocking agents, anticonvulsants, and sedation are often required, further hampering any ability to make an accurate neurologic assessment. Studies have demonstrated that mild therapeutic hypothermia (32–34°C for 24 hours) significantly improves neurologic recovery in unconscious resuscitated cardiac arrest patients. Advanced life support protocols now call for therapeutic cooling to be started in the field or immediately upon hospital arrival (Figure 15–1). In patients who received therapeutic hypothermia, the prognosis is good if they regain consciousness within 72 hours of arrest. Many will recover completely with minimal or no long-term neurologic impairment. Therapeutic hypothermia does not rule out early revascularization, and both strategies should be employed. If coma persists longer than 72 hours, only a minority of patients survive. Those who do will often have persistent severe motor and cognitive deficits. Somatosensory evoked potential testing, measurement of brain-specific enolases, and electroencephalogram data may help to determine prognosis. Decisions about prolonged artificial support of these latter patients are often difficult and require that a variety of medical, ethical, and social factors be taken into consideration.
Proposed management algorithm for out-of-hospital cardiac arrest victims. IABP, intra-aortic balloon pump; ICD, implantable cardioverter-defibrillator; IV, intravenous; LVAD, left ventricular assist device; MAP, mean arterial pressure; PCI, percutaneous coronary intervention; SSEP-EEG, somatosensory evoked potential–electroencephalography; STEMI, ST elevation myocardial infarction; VF, ventricular fibrillation.
Nolan JP, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment and prognostication. A scientific statement from the International Liason Committee on Resuscitation; The American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation
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Peberdy MA, et al. Part 9: post-cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation
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Stub D, et al. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation
Young GB. Neurologic prognosis after cardiac arrest. N Engl J Med.
Noninvasive Evaluation for Structural Heart Disease
Once the patient has recovered to the point that long-term survival seems likely, efforts should be made to define fully the type and extent of underlying cardiac disease.
Although the ECG usually provides the first information available, the initial ECG after defibrillation may be misleading. Transient ST segment elevation in leads with prior Q waves is common and does not always signify a new infarction as the primary cause of the arrest. However, patients with a new ST elevation myocardial infarction are candidates for acute mechanical or pharmacologic reperfusion, and it is better to proceed to catheterization whenever doubt exists. More commonly, the ECG after resuscitation will show such evidence of chronic disease, including old Q waves, conduction defects, or hypertrophy. ST segment and T-wave abnormalities appear in virtually all patients following resuscitation and are of limited significance. The ECG may also be useful in the diagnosis of congenital and acquired LQTS, the Brugada syndrome, preexcitation syndromes, cardiomyopathies, and congenital heart disease.
Echocardiography performed in the coronary care unit can provide a noninvasive assessment of cardiac function and anatomy shortly after resuscitation. An early, two-dimensional echocardiogram can provide valuable information about chamber size, wall thickness, valvular abnormalities, coronary artery anomalies, and ventricular function. Since myocardial stunning is common after arrest, improvements in ejection fraction over time occur frequently so serial studies are often helpful.
Other noninvasive tests may also be appropriate in some cases. Magnetic resonance imaging is particularly valuable in patients with congenital heart disease including coronary artery anomalies and ARVC with myocarditis. Positron emission tomography, magnetic resonance imaging, and isotope perfusion scans may be useful for assessing viability in regions of poor ventricular function. Preserved viability may influence decisions concerning the appropriateness of any attempts at revascularization.
Invasive Evaluation for Structural Heart Disease
Cardiac catheterization provides the most complete assessment of the structure, function, and blood supply of the heart, and it should be performed in virtually all survivors of cardiac arrest. Coronary artery disease is found in about 80% of cardiac arrest patients in the United States and Europe.
The prognosis of a patient who survives a cardiac arrest in the acute phase of a myocardial infarction is determined by the total amount of ventricular damage, the severity of residual ischemia, and the completeness of recovery from any noncardiac complications of the arrest. Treatment of these patients should be similar to that for other acute infarct patients, and special steps to define long-term antiarrhythmic therapy are not required. The role of ischemia in cardiac arrest patients without new Q-wave infarction is controversial. As noted earlier, “high risk” coronary artery lesions are often seen on coronary angiograms in cardiac arrest survivors and at autopsy in those who suffered sudden death. If these lesions are seen in patients with totally normal ventricular function, ischemia from these lesions alone may be responsible for the arrest. Correcting the ischemia through revascularization is the most appropriate—and sometimes the only required—therapy. More commonly, both a potential for acute ischemia and a fixed scar will be present. Transient ischemia may be a trigger for the arrhythmia. Since other triggers may exist, therapy should consider both the ischemia trigger and the underlying substrate.
A variety of arrhythmias can cause cardiac arrest and sudden death. Supraventricular arrhythmias with rapid ventricular rates and primary bradyarrhythmias are infrequent causes of cardiac arrest. However, it is important to identify patients with these arrhythmias because they will require a different therapeutic approach. Ventricular tachycardia and ventricular fibrillation are the most common causes of out-of-hospital cardiac arrest, and the evaluation and treatment of these arrhythmias will be the focus of the rest of this chapter.
The role of noninvasive testing in patients who have suffered cardiac arrest is limited because a history of cardiac arrest has already placed them in a high-risk group. Noninvasive tests, however, are often used to assess the risk for future events in patients with known cardiac disease.
Exercise testing may be useful in some cases of exercise-induced ventricular tachycardia or in some patients with cardiac arrest to determine the presence of inducible ischemia. Abnormal prolongation of the QT interval in patients with LQTS and the appearance of arrhythmias in patients with congenital heart block may also be useful markers of future risk. In most cases, however, exercise testing is used to provide information about the potential for ischemia, rather than to diagnose the mechanism of arrhythmia or to guide therapy.
Ambulatory ECG monitoring is rarely useful in cardiac arrest survivors, but the presence of frequent and complex ventricular premature beats and abnormal heart rate variability are risk factors for sudden death during follow-up in patients with many forms of heart disease. In population studies, frequent or complex ventricular ectopy is associated with an increased risk of both sudden and nonsudden cardiac death. Unfortunately, the prognostic value of ambulatory ECG monitoring data in any individual patient is limited by poor day-to-day reproducibility of the data. The use of antiarrhythmic drug therapy guided by suppression of ventricular ectopic activity has not been shown to improve survival. Other noninvasive tests have been used to risk stratify patients. Tests that assess microvolt T-wave alternans during exercise, late potentials on a signal averaged ECG, heart rate variability, and baroreceptor sensitivity have been proposed, but their value in individual patients is controversial.
Invasive evaluation involves a baseline electrophysiologic study that uses programmed electrical stimulation to initiate and characterize the patient's arrhythmia. As ICDs have become more accepted as the most effective therapy to prevent cardiac arrest, electrophysiologic studies have been relegated to a secondary role. They are now used to help define an arrhythmia mechanism if either an unusual mechanism of arrhythmia or an arrhythmia that might be susceptible to ablation is suspected. The ability to identify an effective antiarrhythmic drug by serial testing is limited, and the failure rate of drug therapy selected by the technique is unacceptably high. However, electrophysiologic studies may be useful for characterizing the effects of drug therapy on tachycardias. Drug therapy may change the rate of many ventricular tachycardias and can affect defibrillation thresholds. Data obtained from electrophysiologic studies during drug therapy can be used to guide programming of ICDs.