Prodrome, Onset, Arrest, Death
SCD may be presaged by days to months of increasing angina, dyspnea, palpitations, easy fatigability, and other nonspecific complaints. However, these prodromal symptoms are generally predictive of any major cardiac event; they are not specific for predicting SCD.
The onset of the clinical transition, leading to cardiac arrest, is defined as an acute change in cardiovascular status preceding cardiac arrest by up to 1 h. When the onset is instantaneous or abrupt, the probability that the arrest is cardiac in origin is >95%. Continuous electrocardiographic (ECG) recordings fortuitously obtained at the onset of a cardiac arrest commonly demonstrate changes in cardiac electrical activity during the minutes or hours before the event. There is a tendency for the heart rate to increase and for advanced grades of PVCs to evolve. Most cardiac arrests that are caused by VF begin with a run of nonsustained or sustained VT, which then degenerates into VF.
The probability of achieving successful resuscitation from cardiac arrest is related to the interval from onset of loss of circulation to institution of resuscitative efforts, the setting in which the event occurs, the mechanism (VF, VT, PEA, asystole), and the clinical status of the patient before the cardiac arrest. Return of circulation and survival rates as a result of defibrillation decrease almost linearly from the first minute to 10 min. After 5 min, survival rates are no better than 25–30% in out-of-hospital settings. Those settings in which it is possible to institute prompt cardiopulmonary resuscitation (CPR) followed by prompt defibrillation provide a better chance of a successful outcome. However, the outcome in intensive care units and other in-hospital environments is heavily influenced by the patient's preceding clinical status. The immediate outcome is good for cardiac arrest occurring in the intensive care unit in the presence of an acute cardiac event or transient metabolic disturbance, but survival among patients with far-advanced chronic cardiac disease or advanced noncardiac diseases (e.g., renal failure, pneumonia, sepsis, diabetes, cancer) is low and not much better in the in-hospital than in the out-of-hospital setting. Survival from unexpected cardiac arrest in unmonitored areas in a hospital is not much better than that it is for witnessed out-of-hospital arrests. Since implementation of community response systems, survival from out-of-hospital cardiac arrest has improved although it still remains low, under most circumstances. Survival probabilities in public sites exceed those in the home environment.
The success rate for initial resuscitation and survival to hospital discharge after an out-of-hospital cardiac arrest depends heavily on the mechanism of the event. When the mechanism is pulseless VT, the outcome is best; VF is the next most successful; and asystole and PEA generate dismal outcome statistics. Advanced age also adversely influences the chances of successful resuscitation.
Progression to biologic death is a function of the mechanism of cardiac arrest and the length of the delay before interventions. VF or asystole without CPR within the first 4–6 min has a poor outcome even if defibrillation is successful because of superimposed brain damage; there are few survivors among patients who had no life support activities for the first 8 min after onset. Outcome statistics are improved by lay bystander intervention (basic life support—see below) before definitive interventions (advanced life support) especially when followed by early successful defibrillation. In regard to the latter, evaluations of deployment of automatic external defibrillators (AEDs) in communities (e.g., police vehicles, large buildings, airports, and stadiums) are beginning to generate encouraging data. Increased deployment is to be encouraged.
Death during the hospitalization after a successfully resuscitated cardiac arrest relates closely to the severity of central nervous system injury. Anoxic encephalopathy and infections subsequent to prolonged respirator dependence account for 60% of the deaths. Another 30% occur as a consequence of low cardiac output states that fail to respond to interventions. Recurrent arrhythmias are the least common cause of death, accounting for only 10% of in-hospital deaths.
In the setting of acute MI (Chap. 245), it is important to distinguish between primary and secondary cardiac arrests. Primary cardiac arrests are those which occur in the absence of hemodynamic instability, and secondary cardiac arrests are those which occur in patients in whom abnormal hemodynamics dominate the clinical picture before cardiac arrest. The success rate for immediate resuscitation in primary cardiac arrest during acute MI in a monitored setting should exceed 90%. In contrast, as many as 70% of patients with secondary cardiac arrest succumb immediately or during the same hospitalization.
Treatment: Cardiac Arrest
An individual who collapses suddenly is managed in five stages: (1) initial evaluation and basic life support if arrest is confirmed, (2) public access defibrillation (when available), (3) advanced life support, (4) postresuscitation care, and (5) long-term management. The initial response, including confirmation of loss of circulation, followed by basic life support and public access defibrillation, can be carried out by physicians, nurses, paramedical personnel, and trained laypersons. There is a requirement for increasingly specialized skills as the patient moves through the stages of advanced life support, postresuscitation care, and long-term management.
Initial Evaluation and Basic Life Support
Confirmation that a sudden collapse is indeed due to a cardiac arrest includes prompt observations of the state of consciousness, respiratory movements, skin color, and the presence or absence of pulses in the carotid or femoral arteries. For lay responders, the pulse check is no longer recommended. As soon as a cardiac arrest is suspected, confirmed, or even considered to be impending, calling an emergency rescue system (e.g., 911) is the immediate priority. With the development of AEDs that are easily used by nonconventional emergency responders, an additional layer for response has evolved (see below).
Agonal respiratory movements may persist for a short time after the onset of cardiac arrest, but it is important to observe for severe stridor with a persistent pulse as a clue to aspiration of a foreign body or food. If this is suspected, a Heimlich maneuver (see below) may dislodge the obstructing body. A precordial blow, or "thump," delivered firmly with a clenched fist to the junction of the middle and lower thirds of the sternum may occasionally revert VT or VF, but there is concern about converting VT to VF. Therefore, it is recommended to use precordial thumps as a life support technique only when monitoring and defibrillation are available. This conservative application of the technique remains controversial.
The third action during the initial response is to clear the airway. The head is tilted back and the chin lifted so that the oropharynx can be explored to clear the airway. Dentures or foreign bodies are removed, and the Heimlich maneuver is performed if there is reason to suspect that a foreign body is lodged in the oropharynx. If respiratory arrest precipitating cardiac arrest is suspected, a second precordial thump is delivered after the airway is cleared.
Basic life support, more popularly known as CPR, is intended to maintain organ perfusion until definitive interventions can be instituted. The elements of CPR are the maintenance of ventilation of the lungs and compression of the chest. Mouth-to-mouth respiration may be used if no specific rescue equipment is immediately available (e.g., plastic oropharyngeal airways, esophageal obturators, masked Ambu bag). Conventional ventilation techniques during single-responder CPR require that the lungs be inflated twice in succession after every 30 chest compressions. Recent data suggest that interrupting chest compressions to perform mouth-to-mouth respiration may be less effective than a continuous chest compression strategy.
Chest compression is based on the assumption that cardiac compression allows the heart to maintain a pump function by sequential filling and emptying of its chambers, with competent valves maintaining forward direction of flow. The palm of one hand is placed over the lower sternum, with the heel of the other resting on the dorsum of the lower hand. The sternum is depressed, with the arms remaining straight, at a rate of approximately 100 per minute. Sufficient force is applied to depress the sternum 4–5 cm, and relaxation is abrupt.
Automated External Defibrillation (AED)
AEDs that are easily used by nonconventional responders, such as nonparamedic firefighters, police officers, ambulance drivers, trained security guards, and minimally trained or untrained laypersons, have been developed. This advance has inserted another level of response into the cardiac arrest paradigm. A number of studies have demonstrated that AED use by nonconventional responders in strategic response systems and public access lay responders can improve cardiac arrest survival rates. This strategy is based on shortening the time to the first defibrillation attempt while awaiting the arrival of advanced life support.
Advanced Cardiac Life Support (ACLS)
ACLS is intended to achieve adequate ventilation, control cardiac arrhythmias, stabilize blood pressure and cardiac output, and restore organ perfusion. The activities carried out to achieve these goals include (1) defibrillation/cardioversion and/or pacing, (2) intubation with an endotracheal tube, and (3) insertion of an intravenous line. The speed with which defibrillation/cardioversion is achieved is an important element in successful resuscitation, both for restoration of spontaneous circulation and for protection of the central nervous system. Immediate defibrillation should precede intubation and insertion of an intravenous line; CPR should be carried out while the defibrillator is being charged. As soon as a diagnosis of VF or VT is established, a shock of at least 300 J should be delivered when one is using a monophasic waveform device or 120–150 J with a biphasic waveform. Additional shocks are escalated to a maximum of 360 J monophasic (200 J biphasic) if the initial shock does not successfully revert VT or VF. However, it is now recommended that five cycles of CPR be carried out before repeated shocks, if the first shock fails to restore an organized rhythm, or 60–90 s of CPR before the first shock if 5 min has elapsed between the onset of cardiac arrest and ability to deliver a shock (see 2005 update of guidelines for cardiopulmonary resuscitation and emergency cardiac care at http://circ.ahajournals.org/content/112/24_suppl.toc).
Epinephrine, 1 mg intravenously, is given after failed defibrillation, and attempts to defibrillate are repeated. The dose of epinephrine may be repeated after intervals of 3–5 min (Fig. 273-3A). Vasopressin (a single 40-unit dose given IV) has been suggested as an alternative to epinephrine.
A. The algorithm of ventricular fibrillation or pulseless ventricular tachycardia begins with defibrillation attempts. If that fails, it is followed by epinephrine and then antiarrhythmic drugs. See text for details. B.The algorithms for bradyarrhythmia/asystole (left) or pulseless electrical activity (right) are dominated first by continued life support and a search for reversible causes. Subsequent therapy is nonspecific and is accompanied by a low success rate. See text for details. CPR, cardiopulmonary resuscitation; MI, myocardial infarction.
If the patient is less than fully conscious upon reversion or if two or three attempts fail, prompt intubation, ventilation, and arterial blood gas analysis should be carried out. Ventilation with O2 (room air if O2 is not immediately available) may promptly reverse hypoxemia and acidosis. A patient who is persistently acidotic after successful defibrillation and intubation should be given 1 meq/kg NaHCO3 initially and an additional 50% of the dose repeated every 10–15 min. However, it should not be used routinely.
After initial unsuccessful defibrillation attempts or with persistent/recurrent electrical instability, antiarrhythmic therapy should be instituted. Intravenous amiodarone has emerged as the initial treatment of choice (150 mg over 10 min, followed by 1 mg/min for up to 6 h and 0.5 mg/min thereafter) (Fig. 273-3A). For cardiac arrest due to VF in the early phase of an acute coronary syndrome, a bolus of 1 mg/kg of lidocaine may be given intravenously as an alternative, and the dose may be repeated in 2 min. It also may be tried in patients in whom amiodarone is unsuccessful. Intravenous procainamide (loading infusion of 100 mg/5 min to a total dose of 500–800 mg, followed by continuous infusion at 2–5 mg/min) is now rarely used in this setting but may be tried for persisting, hemodynamically stable arrhythmias. Intravenous calcium gluconate is no longer considered safe or necessary for routine administration. It is used only in patients in whom acute hyperkalemia is known to be the triggering event for resistant VF, in the presence of known hypocalcemia, or in patients who have received toxic doses of calcium channel antagonists.
Cardiac arrest due to bradyarrhythmias or asystole (B/A cardiac arrest) is managed differently (Fig. 273-3B). The patient is promptly intubated, CPR is continued, and an attempt is made to control hypoxemia and acidosis. Epinephrine and/or atropine are given intravenously or by an intracardiac route. External pacing devices are used to attempt to establish a regular rhythm. The success rate may be good when B/A arrest is due to acute inferior wall myocardial infarction or to correctable airway obstruction or drug-induced respiratory depression or with prompt resuscitation efforts. For acute airway obstruction, prompt removal of foreign bodies by the Heimlich maneuver or, in hospitalized patients, by intubation and suctioning of obstructing secretions in the airway is often successful. The prognosis is generally very poor in other causes of this form of cardiac arrest, such as end-stage cardiac or noncardiac diseases. Treatment of PEA is similar to that for bradyarrhythmias, but its outcome is also dismal.
This phase of management is determined by the clinical setting of the cardiac arrest. Primary VF in acute MI (not accompanied by low-output states) (Chap. 245) is generally very responsive to life support techniques and easily controlled after the initial event. In the in-hospital setting, respirator support is usually not necessary or is needed for only a short time, and hemodynamics stabilize promptly after defibrillation or cardioversion. In secondary VF in acute MI (those events in which hemodynamic abnormalities predispose to the potentially fatal arrhythmia), resuscitative efforts are less often successful, and in patients who are successfully resuscitated, the recurrence rate is high. The clinical picture and outcome are dominated by hemodynamic instability and the ability to control hemodynamic dysfunction. Bradyarrhythmias, asystole, and PEA are commonly secondary events in hemodynamically unstable patients. The in-hospital phase of care of an out-of-hospital cardiac arrest survivor is dictated by specific clinical circumstances. The most difficult is the presence of anoxic encephalopathy, which is a strong predictor of in-hospital death. A recent addition to the management of this condition is induced hypothermia to reduce metabolic demands and cerebral edema.
The outcome after in-hospital cardiac arrest associated with noncardiac diseases is poor, and in the few successfully resuscitated patients, the postresuscitation course is dominated by the nature of the underlying disease. Patients with end-stage cancer, renal failure, acute central nervous system disease, and uncontrolled infections, as a group, have a survival rate of <10% after in-hospital cardiac arrest. Some major exceptions are patients with transient airway obstruction, electrolyte disturbances, proarrhythmic effects of drugs, and severe metabolic abnormalities, most of whom may have a good chance of survival if they can be resuscitated promptly and stabilized while the transient abnormalities are being corrected.
Long‐Term Management after Survival of Out‐of-Hospital Cardiac Arrest
Patients who survive cardiac arrest without irreversible damage to the central nervous system and who achieve hemodynamic stability should have diagnostic testing to define appropriate therapeutic interventions for their long-term management. This aggressive approach is driven by the fact that survival after out-of-hospital cardiac arrest is followed by a 10–25% mortality rate during the first 2 years after the event, and there are data suggesting that significant survival benefits can be achieved by prescription of an implantable cardioverter-defibrillator (ICD).
Among patients in whom an acute ST elevation MI, or transient and reversible myocardial ischemia, is identified as the specific mechanism triggering an out-of-hospital cardiac arrest, the management is dictated in part by the transient nature of life-threatening arrhythmia risk during the acute coronary syndrome (ACS) and in part by the extent of permanent myocardial damage that results. Cardiac arrest during the acute ischemic phase is not an ICD indication, but survivors of cardiac arrest not associated with an ACS do benefit. In addition, patients who survive MI with an ejection fraction less than 30–35% appear to benefit from ICDs.
For patients with cardiac arrest determined to be due to a treatable transient ischemic mechanism, particularly with higher EFs, catheter interventional, surgical, and/or pharmacologic anti-ischemic therapy is generally accepted for long-term management.
Survivors of cardiac arrest due to other categories of disease, such as the hypertrophic or dilated cardiomyopathies and the various rare inherited disorders (e.g., right ventricular dysplasia, long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and so-called idiopathic VF), are all considered ICD candidates.