TREATMENT Cardiac Arrest
An individual who collapses suddenly is managed in five stages: (1) initial evaluation and basic life support if cardiac 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.
INITIAL EVALUATION AND BASIC LIFE SUPPORT Confirmation that a sudden collapse with loss of consciousness (LOC) is 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 because it is unreliable. 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).
Careful attention to the respiratory status after abrupt LOC is important. Although normal breathing or tachypnea after LOC makes cardiac arrest less likely, gasping respiratory movements may persist during a true cardiac arrest, and their presence should not deter appropriate responses. In fact, continued gasping is considered a good prognostic sign for successful outcome. It is also 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 initial and primary element of CPR is maintenance of perfusion until spontaneous circulation can be restored. Closed chest cardiac compression maintains a pump function by sequential filling and emptying of the 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 100 per minute. Sufficient force is applied to depress the sternum 4–5 cm, and relaxation is abrupt.
Until recently, providing ventilation of the lungs by mouth-to-mouth respiration was used if no specific rescue equipment was immediately available (e.g., plastic oropharyngeal airways, esophageal obturators, masked Ambu bag). However, ventilatory support during CPR has yielded to evidence that continuous chest compressions (“hands only” CPR) results in better outcomes. Compressions are interrupted only for single shocks from an AED when available, with 2 min of CPR between each single shock.
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. The rapidity with which defibrillation/cardioversion is achieved is an important element for successful resuscitation, both for ROSC and for protection of the central nervous system. Chest compressions should be carried out while the defibrillator is being charged. As soon as a diagnosis of VF or VT is established, a biphasic waveform shock of 150–200 J (360 J if a monophasic waveform device is used) should be delivered. If 5 min has elapsed between collapse and first contact with the victim, there is some evidence that 60–90 s of CPR before the first shock may improve probability of survival without neurologic damage. If the initial shock does not successfully revert VT or VF, chest compression at a rate of 100 per minute is resumed for 2 min, and then a second shock is delivered. Multiple shocks given in sequence are no longer recommended, in order to minimize interruptions of chest compressions. This sequence is continued until personnel capable of, and equipped for, advanced life support are available, although not much data support the notion that shocks and chest compressions alone will revert VF after three shocks have failed.
ADVANCED CARDIAC LIFE SUPPORT (ACLS) ACLS is intended to achieve and maintain organ perfusion and adequate ventilation, control cardiac arrhythmias, and stabilize blood pressure and cardiac output. 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.
As in basic life support, the major emphasis during ACLS is minimizing interruptions of chest compressions until ROSC is achieved. After two or three unsuccessful defibrillation attempts, epinephrine, 1 mg IV, is given and attempts to defibrillate are repeated. The dose of epinephrine may be repeated after intervals of 3–5 min (Fig. 327-3A). Vasopressin (a single 40-unit dose given IV) has been suggested as an alternative to epinephrine.
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. Quantitative waveform capnography is now recommended for confirmation and monitoring of endotracheal tube placement. A patient who is persistently acidotic after successful defibrillation and intubation or had acidosis prior to arrest, may 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. 327-3A). 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. 327-3B). The patient is promptly intubated, CPR is continued, and an attempt is made to control hypoxemia and acidosis and identify other reversible causes. Epinephrine may be given intravenously or by an intraosseous route. Atropine is no longer considered effective for asystole or PEA, but can be used for bradyarrhythmias. External pacing devices are used to attempt to establish a regular rhythm when atropine fails for a bradyarrhythmia, but chronotropic agents given intravenously are now recognized as an equally effective alternative.
The success rate may be good when B/A arrest is due to acute inferior wall MI 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.
POST-CARDIAC ARREST SYNDROME AND POSTRESUSCITATION CARE After return of spontaneous or stable assisted circulation, attention shifts to the diagnostic and therapeutic elements of the post-cardiac arrest syndrome. This recently developed clinical classification emerged from the organization of the elements of injury following cardiac arrest into a multidisciplinary continuum. The four components of post-cardiac arrest syndrome include brain injury, myocardial dysfunction, systemic ischemia/reperfusion responses, and control of persistent precipitating factors. The therapeutic goal is to maintain a stable electrical, hemodynamic, and central nervous system status.
Postresuscitation care is determined by the specific clinical circumstances. The most pressing is the presence of anoxic encephalopathy, which is a strong predictor of in-hospital death and postarrest disability. Mild therapeutic hypothermia is indicated for resuscitated cardiac arrest victims who are hemodynamically stable, but remain comatose. Core body temperature is decreased to 32–34°C, by several available techniques (external and/or internal [core]), as soon as practical after resuscitation and maintained for a minimum of 12–24 h. By reducing metabolic demands and cerebral edema, this intervention improves probability of survival with better neurologic outcome.
Primary VF in acute MI (not accompanied by low-output states) (Chap. 295) 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 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 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 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 EF 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.