Key words
Advanced cardiac life support, Cardiac arrest, Cardiopulmonary resuscitation, Pediatric resuscitation, Post-resuscitation care
Key Points
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Cardiac arrest is a major public health issue worldwide. Despite significant advances in resuscitation science, survival rates remain considerably low. Improvement of patient survival and neurologic outcome relies on the development and implementation of vigorous and evidence-based resuscitation guidelines involving basic life support (BLS), advanced cardiovascular life support, and post–cardiac arrest care.
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In cardiac arrests without hypoxic causes, oxygen content in the lungs at the time of cardiac arrest is usually sufficient for maintaining acceptable arterial oxygen content during the first several minutes of cardiopulmonary resuscitation (CPR). Blood flow rather than arterial oxygen content is the limiting factor for oxygen delivery to coronary, cerebral, and systemic circulation during CPR. Thus rescue breaths are less important than initiating effective chest compressions as soon as possible after sudden cardiac arrest (SCA).
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The mechanism through which chest compressions generate blood flow can be explained by the thoracic or cardiac pump theories. The provision of uninterrupted, high-quality chest compressions after SCA is associated with better survival and neurologic outcomes than delaying chest compressions for airway intervention in both adult and pediatric patients. Circulation, airway, breathing has replaced airway, breathing, circulation.
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A single resuscitative shock should be delivered at the earliest possible opportunity after the recognition of cardiac arrest, followed immediately by the resumption of chest compressions without postshock cardiac rhythm analysis. Outcome studies have failed to demonstrate the benefit of a period of chest compressions before shock or for a series of stacked shocks.
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Vasopressor medications during resuscitation have been de-emphasized in deference to providing uninterrupted, high-quality chest compressions. Standard-dose epinephrine (1 mg every 3-5 minutes) is recommended for patients in cardiac arrest. Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest and has been removed from the adult cardiac arrest algorithm. Steroids combined with a vasopressor bundle or cocktail of epinephrine and vasopressin improved return of spontaneous circulation (ROSC) compared with the use of placebo and epinephrine alone in out-of-hospital cardiac arrest.
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Continuous-flow left ventricular assist devices result in an unconventional, unique physiologic state of hemodynamically stable pulseless electric activity. Assessment of adequate tissue perfusion is the most important factor in determining the need for circulatory assistance such as chest compressions. Total artificial hearts (TAHs) are refractory to chest compressions, antiarrhythmic drugs, and electric therapy. Vasopressor medications are contraindicated because they increase afterload, result in complete hemodynamic collapse with pulmonary edema, and worsen TAH function.
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In consideration of opioid overdose epidemiology, patients with known or suspected opioid addiction who are in cardiac or respiratory arrest should receive intravenous, intramuscular, or intranasal naloxone in addition to standard BLS care.
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For nonshockable rhythms, the essential step will be early detection and correction of potentially reversible underlying causes. Ultrasound technology is used to assess the etiology and the management of these patients, as well as to predict the possibility of ROSC and to justify the termination of resuscitative efforts. However, utilization of this technique should not interfere with other resuscitation efforts such as chest compressions.
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Asphyxiation is a much more common cause of cardiac arrest in infants and children than the primary cardiac event, and airway management and ventilation are therefore more important during the resuscitation of children. However, in order to facilitate training, retention, and implementation of resuscitation guidelines, the pediatric resuscitation guidelines follow similar principles as adult guidelines.
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Targeted temperature management (TTM) applied to comatose survivors of out-of-hospital cardiac arrests has significantly improved the neurologic recovery in those surviving to hospital discharge. A target temperature between 32°C and 36°C is recommended for at least 24 hours, and normothermia (to treat fever) should be maintained beyond this window. Prognostication should not occur until 72 hours after ROSC or, if TTM is provided, 72 hours after completion of TTM.
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Most deaths after SCA in both adults and children typically occur within the first 24 hours. Coordinated postresuscitation care involving access to coronary catheterization capabilities and intensive care management that includes TTM represents the best chance survivors of SCA have for optimal neurologic and cardiac recovery.
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New technologies such as individualized CPR, extracorporeal CPR, controlled automated reper-fusion of the whole body (CARL), and emergency preservation for delayed resuscitation may offer opportunities for patients suffering from cardiac arrest.
Acknowledgment
The editors and publisher would like to thank Drs. Brian P. McGlinch and Roger D. White for contributing a chapter on this topic in the prior edition of this work. It has served as the foundation for the current chapter.
Sudden Cardiac Arrest and Cardiopulmonary Resuscitation
Brief History and Physiologic Considerations
Cardiac arrest is a major public health issue, with more than 500,000 deaths per year in the United States. Seventy percent of out-of-hospital cardiac arrests (OHCAs) occur at home, and approximately 50% are unwitnessed. Despite significant advances in resuscitation science, survival rates remain considerably low for both OHCA and in-hospital cardiac arrest (IHCA). Only 10.4% of adult patients with nontraumatic cardiac arrest who receive resuscitative efforts from emergency medical services (EMS) survive to hospital discharge. IHCA has a better outcome, with 22.3% to 25.5% of adults surviving to hospital discharge. Statistics for Europe are similar, with OHCA as one of the leading causes of death in Europe and an overall survival rate of 2.6% to 10.7%.
Sudden cardiac arrest (SCA) is a complex and dynamic process. Forward systemic arterial blood flow continues after cardiac arrest until the pressure gradient between the aorta and right heart reaches equilibrium. A similar process occurs with forward pulmonary blood flow between the pulmonary artery and the left atrium. As the arteriovenous pressure gradient diminishes, the left heart filling is decreased, right heart filling is increased, and the venous capacitance vessels become increasingly distended. When the arterial and venous pressures reach equilibration (approximately 5 minutes after no-flow cardiac arrest), coronary perfusion and cerebral blood flows stop. The goal of cardiopulmonary resuscitation (CPR) thus is to maintain oxygen and blood supply to vital organs, restore spontaneous circulation, minimize postresuscitation organ injury, and ultimately improve the patient’s survival and neurologic outcome.
The history of CPR traces back to the biblical age. However, the more contemporary approach to CPR dates back to the 1950s. James Elam and Peter Safar showed that the earlier methods of resuscitation with chest-pressure and arm-lift were ineffective, and that mouth-to-mouth ventilation was an easily learned and life-saving approach. William B. Kouwenhoven of Johns Hopkins University is credited with introducing a formalized system of chest compressions. Claude Beck of Case Western Reserve University and Paul Zoll of Beth Israel Hospital introduced defibrillation to break ventricular fibrillation. In 1966 the National Academy of Sciences National Research Council conference generated consensus standards for the performance of CPR and opened the modern era of CPR.
The mechanism through which chest compressions generate blood flow can be explained by the thoracic or cardiac pump theories. The thoracic pump theory postulates that blood flows from the thorax when the intrathoracic vascular pressures exceed extrathoracic pressures. The venous-to-arterial blood flow direction is a result of venous valves that prevent retrograde flow at the thoracic inlet. According to the cardiac pump theory, blood flow is generated as a result of actual compression of the heart between the sternum and the vertebral column. Transesophageal echocardiography (TEE) during CPR in humans allowed direct visualization of changes in cardiac chambers and valve functions during chest compressions, as well as the direction of blood flow. During chest compression, the tricuspid and mitral valves close, the left and right ventricular volumes decrease, and blood is ejected into the arterial system. During the decompression phase of CPR, the pressure gradient between the systemic venous system and thoracic cavity facilitates blood flow into the heart chambers. Systemic blood flow during CPR is dependent on effective chest compressions but also on the venous blood return to the heart. Therefore, even modest increases in the intrathoracic pressure, as might occur with overzealous ventilation during CPR, will impair venous return and negatively impact systemic, coronary, and cerebral perfusions and also reduce the chances of return of spontaneous circulation (ROSC).
Cardiac output during CPR with effective, uninterrupted chest compression is at best 25% to 30% of the normal spontaneous circulation. In cardiac arrests without hypoxic causes (e.g., suffocation, drowning), oxygen content in the lungs at the time of cardiac arrest is usually sufficient for maintaining acceptable arterial oxygen content during the first several minutes of CPR. Blood flow rather than arterial oxygen content is the limiting factor for oxygen delivery to coronary, cerebral, and systemic circulation during CPR. Thus rescue breaths are less important than initiating effective chest compressions as soon as possible after SCA.
Understanding the pathophysiology during SCA and CPR is vitally important. The actual improvement of patient outcome, however, relies on development and implementation of vigorous and evidence-based resuscitation guidelines. The more recent recommendations, the 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (2015 American Heart Association [AHA] Guidelines for CPR and ECC), represent the fourth internationally recognized resuscitation guidelines from the AHA and the European Resuscitation Council; therefore, these guidelines are practiced in many countries and medical specialties. More recently, the guidelines underwent a major updating process change. Instead of updating guidelines every 5 years, the new process involves a continuous evidence evaluation process and annual guidelines update, with the most recent one being the 2017 AHA Guidelines for CPR and ECC update. The intent of this chapter is to review the history, rationale, and current understanding of both basic life support (BLS) and advanced cardiovascular life support (ACLS) techniques based on the most recent updated guidelines.
Basic Life Support
BLS is, according to the Carnegie Safety Institute, the foundation for saving lives after cardiac arrest. Fundamental aspects of adult BLS include immediate recognition of SCA and activation of the emergency response system, early CPR, and rapid defibrillation with an automated external defibrillator (AED). Initial recognition and response to heart attack and stroke are also considered as parts of the BLS. All BLS interventions are time sensitive for preventing SCA, terminating SCA, or supporting circulation until spontaneous circulation is restored. The steps of the adult BLS algorithm for healthcare providers are illustrated in Fig. 86.1 .
The 2015 AHA Guidelines for CPR and ECC on BLS continue to emphasize the simplified universal adult BLS algorithm. The recommended sequence for a single rescuer is to initiate chest compressions before giving rescue breaths (circulation, airway, breathing [C-A-B] rather than airway, breathing, circulation [A-B-C]) to reduce any delay in providing effective chest compressions in adults without any known information of possible asphyxiation as the cause of cardiac arrest. The single rescuer should begin CPR with 30 chest compressions followed by 2 breaths. The guideline, in addition, also emphasizes a simultaneous, choreographed approach to the performance of chest compressions, airway management, rescue breathing, rhythm detection, and shocks (if indicated) by an integrated team of highly trained rescuers in applicable settings such as the hospital environment. With the current rhythm analysis technology, pause of chest compressions may still be required for accurate rhythm analysis, but the compressions should be resumed as soon as possible after rhythm analysis or defibrillation. The key components of high-quality CPR for BLS providers are summarized in Table 86.1 .
| Component | Adults and Adolescents | Children (Age 1 Year to Puberty) | Infants (Age Less Than 1 Year, Excluding Newborns) |
|---|---|---|---|
| Scene safety | Make sure the environment is safe for rescuers and victim | ||
| Recognition of cardiac arrest | Check for responsiveness No breathing or only gasping (i.e., no normal breathing) No definite pulse felt within 10 s (Breathing and pulse check can be performed simultaneously in less than 10 s) | ||
| Activation of emergency response system | If you are alone with no mobile phone, leave the victim to activate the emergency response system and get the AED before beginning CPR Otherwise, send someone and begin CPR immediately; use the AED as soon as it is available | Witnessed collapse Follow steps for adults and adolescents on the left Unwitnessed collapse Give 2 min of CPR Leave the victim to activate the emergency response system and get the AED Return to the child or infant and resume CPR; use the AED as soon as it is available | |
| Compression-ventilation ratio without advanced airway | 1 or 2 rescuers 30:2 | 1 rescuer 30:2 2 or more rescuers 15:2 | |
| Compression-ventilation ratio with advanced airway | Continuous compressions at a rate of 100-120/min Give 1 breath every 6 s (10 breaths/min) | ||
| Compression rate | 100-120/min | ||
| Compression depth | At least 2 inches (5 cm) ∗ | At least one-third AP diameter of chest About 2 inches (5 cm) | At least one-third AP diameter of chest About 1 1⁄2 inches (4 cm) |
| Hand placement | 2 hands on the lower half of the breastbone (sternum) | 2 hands or 1 hand (optional for very small child) on the lower half of the breastbone (sternum) | 1 rescuer 2 fingers in the center of the chest, just below the nipple line 2 or more rescuers 2 thumb–encircling hands in the center of the chest, just below the nipple line |
| Chest recoil | Allow full recoil of chest after each compression; do not lean on the chest after each compression | ||
| Minimizing interruptions | Limit interruptions in chest compressions to less than 10 s | ||
∗ Compression depth should be no more than 2.4 inches (6 cm).
Recognition of Sudden Cardiac Arrest
The necessary first step in the management of cardiac arrest is its immediate recognition. Studies have shown that both lay rescuers and healthcare providers have difficulty detecting a weak pulse. The healthcare provider should take no more than 10 seconds to check for a pulse and, if the rescuer does not definitely feel a pulse within that time period, start chest compressions. Ideally, the pulse check is performed simultaneously with the examination for breathing or gasping, to minimize delay in the detection of cardiac arrest and initiation of CPR. Cardiac arrest victims sometimes present with seizure-like activity or agonal gasps that can confuse potential rescuers. If the victim is unresponsive with absent or abnormal breathing, the rescuer should assume that the victim is in cardiac arrest.
Bystander Cardiopulmonary Resuscitation
For victims of OHCA, the key determinants of survival are timely performance of high-quality bystander CPR and, in the presence of any of the shockable rhythms of ventricular fibrillation or pulseless ventricular tachycardia (VT), defibrillation. Similarly, for IHCA, the important provider-dependent determinants of survival are early defibrillation for shockable rhythms and high-quality CPR, along with recognition and response to deteriorating patients before an arrest. The implication of timely CPR is discussed in the next section of this chapter. The components of high-quality CPR include compressing the chest at an adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in compressions, and avoiding excessive ventilation.
As previously described, chest compressions create blood flow by increasing the intrathoracic pressure and directly compressing the heart. The 2015 AHA Guidelines for CPR and ECC recommended a chest compression rate of 100 to 120/min (updated from at least 100/min), and a chest compression depth for adults of at least 2 inches (5 cm) but not greater than 2.4 inches (6 cm). Despite the “push hard and push fast” recommendation, most CPR feedback devices have shown that compressions are more often too shallow than too deep. In clinical practice, the compression depth may be difficult to judge without the use of feedback devices, and identification of upper limits of compression depth may be challenging. The addition of an upper limit of compression rate is based on a large registry study analysis associating extremely rapid compression rates (greater than 140/min) with inadequate compression depth. Overzealous and rapid chest compressions also compromise chest recoil and venous return, and can potentially have adverse effects on patient survival and outcome.
The total number of compressions delivered during resuscitation is an important determinant of ROSC and survival with good neurologic function from cardiac arrest. The number of compressions delivered is affected by the compression rate (the frequency of chest compressions per minute) and by the compression fraction (the portion of total CPR time during which compressions are performed). Obviously, increases in compression rate and fraction increase the total number of compressions delivered. Compression fraction is improved by reducing the number and duration of any interruptions in compressions (such as securing the airway, delivering rescue breaths, or allowing AED analysis).
Compression-only CPR is easy for an untrained rescuer to perform and can be more effectively guided by dispatchers over the telephone. Moreover, survival rates from adult cardiac arrests of cardiac etiology are similar with either compression only CPR or CPR with both compressions and rescue breaths when provided before EMS arrival. However, for the trained lay rescuer who is able, the recommendation remains for the rescuer to perform both compressions and breaths, especially for victims with asphyxiation causes of cardiac arrest or prolonged CPR. The same emphasis on rescue breathing should also apply to the pediatric population. All lay rescuers should, at a minimum, provide chest compressions for victims of cardiac arrest. The rescuer should continue CPR until an AED arrives and is ready for use, EMS providers take over care of the victim, or the victim starts to move.
The 2015 AHA Guidelines for CPR and ECC emphasize the initiation of chest compressions before ventilation (i.e., a change in the sequence from A-B-C to C-A-B). The prioritization of circulation (C) over ventilation reflected the overriding importance of blood flow generation for successful resuscitation and practical delays inherent to initiation of rescue breaths (B). Physiologically, in most cases of SCA, the need for assisted ventilation is a lower priority because of the availability of adequate arterial oxygen content at the time of a SCA. The presence of this oxygen and its renewal through gasping and chest compressions (provided there is a patent airway) also supported the use of compression-only CPR and the use of passive oxygen delivery.
Shock First or Chest Compressions?
Previous guidelines recommended a period of chest compressions before attempting defibrillation in unwitnessed cardiac arrests or when CPR had been delayed longer than 4 minutes. However, two recent randomized control trials failed to demonstrate a benefit (ROSC or hospital discharge) when CPR was performed before defibrillation. Thus the 2015 AHA Guidelines for CPR and ECC recommend that for adult witnessed cardiac arrests when an AED is immediately available, the defibrillator should be used as soon as possible. For adults with unmonitored cardiac arrest or for whom an AED is not immediately available, it is reasonable that chest compressions be initiated while the defibrillator equipment is being retrieved and applied, and that defibrillation, if indicated, be attempted as soon as the device is ready for use.
Automated External Defibrillators and Manual Defibrillation
Ventricular fibrillation (VF) and pulseless VT are the most common cardiac arrhythmias encountered during witnessed cardiac arrest in adults. CPR prolongs tissue viability and the duration of VF by providing oxygen and energy substrate, but cannot convert the arrhythmia to an organized rhythm in most circumstances. Defibrillation delivers an electrical current passing through the myocardium to interrupt disorganized cardiac activity and restore an organized cardiac rhythm.
The first AED was introduced in 1979. When it is applied to an individual with possible SCA, the AED analyzes the cardiac rhythm, and then automatically attempts defibrillation if it is VF or rapid VT. A trained rescuer needs to simply apply the defibrillator pads to the patient’s chest, activate the AED, and deliver the shock through the push of a button when prompted to do so by the AED. Thus the purpose is to have early defibrillation more readily available through trained bystanders, such as security guards, police, and the general public.
When a standard manual defibrillator is used in resuscitation, the rescuer needs to interpret the rhythm and shock when appropriate. If a monophasic defibrillator is available, then a single 360 joule (J) shock should be delivered. With biphasic defibrillators, a much lower energy level (150-200 J) is usually sufficient to terminate the arrhythmia due to its ability to compensate and adjust for the patient’s impedance. If the rescuer is unfamiliar with the waveform used or the manufacturer recommendations, then the maximal available energy should be used as the default energy. There is no evidence indicating superiority of one biphasic waveform design or energy level for the termination of VF with the first shock. For subsequent shocks, it is reasonable to select fixed versus escalating energy based on the specific manufacturer’s instructions.
The same protocol used with the AED should be applied when using the manual defibrillator: (1) emphasis is placed on delivering uninterrupted chest compressions while defibrillator pads are being applied and for periods when rhythm analysis is not occurring; (2) chest compressions are immediately resumed after shock delivery; (3) cardiac rhythm is reanalyzed as indicated after 2 minutes of chest compressions and rescue breathing; and (4) defibrillation is attempted only for VF and rapid VT.
Single versus Stacked Defibrillation
The 2015 AHA Guidelines for CPR and ECC recommended a 2-minute period of chest compressions after each shock instead of immediate successive shocks for persistent VF. The rationale for this is that when VF is terminated, a brief period of asystole or pulseless electrical activity (PEA) typically ensues and a perfusing rhythm is unlikely to be present immediately, necessitating chest compressions to provide organ perfusion and circulation of ACLS drugs. No difference in the 1-year survival or frequency of VF recurrence was shown when a single shock protocol with 2 minutes of CPR between successive shocks was compared against a previous resuscitation protocol employing three initial stacked shocks with 1 minute of CPR between subsequent shocks. A recent study demonstrated that in monitored in-hospital VF/VT arrests, expeditious defibrillation with use of stacked shocks is associated with a higher rate of ROSC and survival to hospital discharge. Without further data, current AHA guidelines recommend that a single-shock strategy (as opposed to stacked shocks) is reasonable for defibrillation. Stacked defibrillation is considered only during cardiac surgery or in the cardiac catheterization laboratory where invasive monitoring and defibrillation pads are in place already.
Determination of Efficiency of Cardiopulmonary Resuscitation
Immediately after cardiac arrest, when minute ventilation is constant and carbon dioxide (CO 2 ) production is unchanged, the changes in the partial pressure of end-tidal CO 2 (PETCO 2 ) can serve as a reliable surrogate for pulmonary blood flow and cardiac output. This has been proven extensively by animal and human studies during cardiac arrest and CPR and after ROSC. Monitoring of both PETCO 2 by quantitative waveform capnography with controlled ventilation and systemic arterial pressure by invasive monitoring should provide optimal assessment of the efficiency of CPR. These parameters can be monitored continuously, without interrupting chest compressions. An abrupt increase in any of these parameters is a sensitive indicator of ROSC. The 2015 AHA Guidelines for CPR and ECC endorse this monitoring as a class I recommendation for adults with SCA with an endotracheal tube (ETT) or supraglottic airway (SGA) device in place. In addition, coronary perfusion pressure, arterial relaxation pressure, and central venous oxygen saturation can assist in determination of the efficiency of CPR, although these monitoring techniques require more complex catheters or devices. Currently there are no clinical trials that have studied whether titrating resuscitative efforts to a single or combined set of physiologic parameters during CPR results in improved survival or neurologic outcome. However, the 2010 AHA Guidelines for CPR and ECC recommended that PETCO 2 should be maintained above 10 mm Hg, and mathematical models suggest a cumulative maximum PETCO 2 above 20 mm Hg at all time points measured between 5 and 10 minutes postintubation best predicted ROSC.
Update to Airway Management and Ventilation in Cardiac Arrest
When cardiac arrest occurs, adequate oxygen delivery is required to restore the energy state of the heart as well as other vital organs, and consequently ventilation becomes an essential part of the resuscitation. However, it also needs to be emphasized that during the first few minutes after cardiac arrest, oxygen delivery to tissues with CPR is limited more by blood flow and low cardiac output than arterial oxygen content. Low cardiac output associated with CPR results in low oxygen uptake from the lungs that, in turn, reduces the need to ventilate the patient during this low-flow state. Thus chest compressions are the priority intervention, unless the cardiac arrest is due to asphyxiation, drowning, or suffocation, which are the only circumstances in which ventilation must be provided before chest compressions.
Healthcare providers must determine the best way to support ventilation and oxygenation. Options include standard bag-mask ventilation versus placement of an advanced airway (i.e., ETT or SGA device). Bag-mask ventilation with a head tilt–chin lift or head tilt–jaw thrust maneuver is recommended for initial airway control in most circumstances. There is inadequate evidence to show a difference in survival or favorable neurologic outcome with the use of bag-mask ventilation compared with endotracheal intubation or other advanced airway devices. There is also inadequate evidence favoring the use of endotracheal intubation compared with other advanced airway devices. Thus 2015 AHA/Guidelines for CPR and ECC recommend that either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital settings, assuming that providers have ongoing experience to insert the airway and verify proper position with minimal interruption in chest compressions. The choice of bag-mask device versus advanced airway insertion is determined by the skill and experience of the provider.
Regarding the inspired oxygen concentration, the 2015 AHA Guidelines for CPR and ECC support providing the maximal inspired oxygen concentration during CPR. Since oxygen delivery is dependent on both blood flow and arterial oxygen content and blood flow is typically limited during CPR, it is theoretically important to maximize the oxygen content of arterial blood by maximizing inspired oxygen concentration. Evidence for the detrimental effects of hyperoxia that may exist in the immediate post–cardiac arrest period should not be extrapolated to the low-flow state of CPR, where oxygen delivery is unlikely to exceed demand or cause an increase in tissue PO 2 . Therefore, until further data are available, physiology and expert consensus support providing the maximal inspired oxygen concentration during CPR.
After ETT placement, it is very important to confirm its correct placement, although this could be very challenging due to the patient’s body habitus, low-flow status, and distraction from other resuscitative tasks. In addition to observation of chest rise and auscultation of the lungs and stomach, continuous waveform capnography is recommended as the most reliable method of confirming and monitoring correct placement of an ETT. However, false-positive results (CO 2 detection with esophageal intubation) can still occur, especially within the first few breaths due to air/CO 2 insufflation of the stomach during bag-mask ventilation. False-negative results (i.e., absent exhaled CO 2 in the presence of tracheal intubation) can occur in the setting of pulmonary embolism (PE), low cardiac output, or severe obstructive pulmonary disease. If continuous waveform capnography is not available, a nonwaveform CO 2 detector, fiberoptic scope, esophageal detector, or ultrasound device used by an experienced operator are reasonable alternatives.
If bag-mask ventilation is chosen, 2 breaths are delivered after 30 chest compressions during one- and two-person CPR, providing that the rescuer(s) is(are) trained in CPR. Each breath is delivered over approximately 1 second. After placement of an advanced airway, it is recommended to provide 1 breath every 6 seconds (10 breaths/min) while continuous chest compressions are being performed. Extreme caution should be taken to avoid excessive airway pressure that will compromise venous return in cardiac arrest patients, as hyperventilation is common during enthusiastic resuscitation.
Advanced Cardiac Life Support: Management of Cardiac Arrest
BLS, ACLS, and post–cardiac arrest care are integral steps in the AHA’s “chain of survival” for patients suffering from cardiac arrest. CPR almost invariably necessitates rapid progression to ACLS interventions and follow-up care. There is overlap between these steps, as each stage of care progresses to the next, but generally ACLS comprises the level of care between BLS and post–cardiac arrest care. The 2015 AHA Guidelines for CPR and ECC adult cardiac arrest algorithm is illustrated in Fig. 86.2 . This section reviews the different interventions for managing cardiac arrest patients based on the presenting ECG rhythm, medications used during cardiac arrest, special situations of cardiac arrest, and new technologies developed to facilitate resuscitation and improve the patient’s survival.
Asystole
Asystole is the complete and sustained absence of electrical activity and portends extremely poor prognosis. Management of a patient in cardiac arrest with asystole follows the same pathway as management of PEA (as discussed later). The top priorities are also similar: following the steps in the ACLS Pulseless Arrest Algorithm and identifying and correcting any treatable, underlying causes for the asystole. In most patients, asystole is irreversible, but a brief trial of resuscitation, beginning with effective chest compressions, oxygen therapy, and intravenous (IV) epinephrine, is indicated particularly in the setting of witnessed cardiac arrest. Atropine is no longer recommended for treating asystole. Asystole should be differentiated from agonal bradycardia and fine ventricular fibrillation.
Pulseless Electrical Activity
PEA refers to the presence of organized electrical activity without a palpable pulse. Priority must be given to identifying possible reversible causes of PEA, which is frequently referred to as the five Hs (Hypoxia, Hypovolemia, Hypothermia, Hyper- or Hypokalemia, Hydrogen ions or acidosis) and Ts (Tamponade, Tension pneumothorax, Toxins, Thrombosis Pulmonary, and Thrombosis Coronary). Those causes are first suspected for each patient’s special circumstance. Severe hypoxia in respiratory emergencies can result in PEA. In the traumatized patient, hypovolemia, cardiac tamponade, and tension pneumothorax are possible causes of cardiac arrest and must be considered and acutely treated. Unanticipated cardiac arrest occurring in the intraoperative and postoperative periods should include acute massive pulmonary thromboembolism or air emboli as possible causes. Electrolyte and metabolic derangements such as severe hyperkalemia, metabolic acidosis, or drug (e.g., digitalis, β-blockers, calcium channel blockers, tricyclic antidepressants) overdose frequently presents as idioventricular rhythms. In every circumstance, prompt initiation of chest compressions and the administration of 1 mg epinephrine are recommended as temporizing measures until more definitive therapy can be provided once the cause for the PEA is identified. Each of these scenarios has an associated intervention unique to that situation. Asystole or VF can develop if PEA is not corrected.
Pulseless Ventricular Tachycardia or Ventricular Fibrillation
Pulseless VT and VF are shockable rhythms and hence the most treatable causes of cardiac arrest, yielding the greatest likelihood of ROSC and long-term survival in both in-hospital and out-of-hospital settings. Early defibrillation, not pharmacologic intervention, is responsible for the improved survival after VF cardiac arrest. Therefore, AEDs are placed in public locations to ensure early defibrillation can be performed by rescuers.
When a pulseless VT or VF arrest occurs, defibrillation should be performed at the earliest opportunity. Chest compressions should be immediately resumed after the delivery of shock and continued for 2 minutes before reassessing the underlying cardiac rhythm, unless obvious evidence for ROSC occurs. No evidence supports one biphasic waveform over another. Defibrillation energies should be increased until VF is terminated. In circumstances in which pulseless VT or VF is terminated with defibrillation but pulseless VT or VF recurs, defibrillation should use the previously successful energy level.
If ROSC does not occur after an initial defibrillatory attempt, then five cycles of CPR consisting of 30 compressions to 2 ventilations (nonintubated patient) should be performed before recheck of rhythm. Placement of a SGA device or endotracheal intubation can be considered in this interval. Peripheral IV access should be attempted if not already established without interruption of the chest compressions.
Resuscitation Medications During Cardiac Arrest
Epinephrine
Epinephrine produces beneficial effects in patients during cardiac arrest, primarily due to its α-adrenergic effects increasing coronary perfusion pressure and cerebral perfusion pressure during CPR. The β-adrenergic effects of epinephrine are controversial because they may increase myocardial work and reduce subendocardial perfusion. Thus standard-dose epinephrine (1 mg every 3-5 minutes) is recommended for patients in cardiac arrest. High-dose epinephrine is not recommended for routine use in cardiac arrest. The exceptions to this recommendation are special circumstances requiring higher or repeated doses of epinephrine, such as in patients with β-blocker overdose, calcium channel blocker overdose, or when epinephrine is titrated to real-time physiologically monitored parameters.
Regarding the timing of epinephrine administration, multiple trials showed the early administration of epinephrine in nonshockable rhythms (asystole or PEA) was associated with increased ROSC, survival to hospital discharge, and neurologically intact survival. For shockable rhythms (VF or pulseless VT), there is insufficient evidence to make a recommendation as to the optimal timing of epinephrine, particularly in relation to defibrillation. Therefore early administration of epinephrine is recommended after the onset of cardiac arrest caused by an initial nonshockable rhythm.
Vasopressin
Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction. Studies compared multiple doses of standard-dose epinephrine with multiple doses of vasopressin (40 units IV) or vasopressin in combination with epinephrine after OHCA and showed no benefit with the use of vasopressin solely or in combination with epinephrine for ROSC or survival to discharge with or without good neurologic outcome. Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest and thus has been removed from the adult cardiac arrest algorithm.
Antiarrthymia Medications
The role of antiarrhythmic medications during shock-refractory VF/pulseless VT is to facilitate the restoration and maintenance of a spontaneous perfusing rhythm in concert with the shock termination of VF, instead of directly converting VF/pulseless VT to an organized perfusing rhythm. Some antiarrhythmic drugs have been associated with increased rates of ROSC and hospital admission, but none have yet been proven to increase long-term survival or survival with good neurologic outcome. Thus the 2015 AHA Guidelines for CPR and ECC on ACLS recommend that amiodarone may be considered for VF/pulseless VT that is unresponsive to CPR, defibrillation, and a vasopressor therapy; and lidocaine may be considered as an alternative to amiodarone. Routine use of magnesium for VF/pulseless VT is not recommended in adult patients, nor is the routine use of sodium bicarbonate for any patient in cardiac arrest.
Steroids
The use of steroids in cardiac arrest has been assessed in both IHCA and OHCA settings. In IHCA, patients administered steroids combined with a vasopressor bundle or cocktail of epinephrine and vasopressin had improved ROSC compared with patients given a saline placebo and epinephrine. However, further studies are needed before recommending the routine use of this therapeutic strategy. For patients with OHCA, studies showed inconsistent benefit of use of steroids alone during CPR and thus routine use is not recommended.
Cardiopulmonary Resuscitation in Patients With Mechanical Circulatory Support
Cardiac arrest in patients on mechanical circulatory support (MCS) has become a much more common clinical scenario due to the increased use of this therapy in patients with end-stage heart failure. Because of the unique characteristics of mechanical support, these patients have physical findings that cannot be interpreted the same as for patients without MCS. This section briefly describes the common types of MCS devices that healthcare providers may encounter and presents expert, consensus-based recommendations from the recent AHA guidelines for the evaluation and resuscitation of adult patients with MCS, and suspected cardiovascular collapse or cardiac arrest.
MCS with ventricular assist devices (VADs) can support function of the left ventricle (LV), the right ventricle (RV), or both ventricles with a biventricular assist device. A total artificial heart (TAH) replaces the heart itself. Most patients who are discharged home with MCS currently have a durable left ventricular VAD (LVAD). Continuous-flow LVADs are the more current generation of VADs. It results in an unconventional, unique physiologic state of hemodynamically stable PEA, which we refer to in this population as pseudo-PEA. Vital signs such as noninvasive blood pressure or oxygen saturation may be difficult to obtain. These factors can easily confuse healthcare providers rendering care to these patients. Lack of a pulse alone in a patient with a continuous-flow LVAD is common and cannot be used as a means to determine whether a patient is in cardiac arrest or a low-flow, low-perfusion state.
Assessment of adequate tissue perfusion is the most important factor in determining the need for circulatory assistance such as chest compressions. Clinical findings such as skin color and capillary refill are reasonable predictors of the presence of adequate flow and perfusion. If an LVAD is definitively confirmed by a trained person and there are no signs of life, bystander CPR, including chest compressions, is recommended. Many tachyarrhythmias are tolerated well in patients with an LVAD, although they can affect RV filling. Similar to the decision made for patients without VADs, the decision to cardiovert or to defibrillate a patient with an LVAD with VT or VF is based on the adequacy of mental status and perfusion. Fig. 86.3 outlines consensus-derived recommendations for first-responder assessment of a patient with an LVAD.
For patients with a TAH, the native ventricles are removed completely; therefore, there is no electric depolarization and therefore no detectable ECG tracing. Chest compressions are ineffective because the mechanical ventricles are rigid and cannot be compressed. Antiarrhythmic drugs and electric therapy (e.g., pacing, defibrillation/cardioversion) are also futile for similar reasons. Standard vasopressor drugs used in ACLS such as epinephrine or vasopressin are contraindicated because they increase afterload, result in complete hemodynamic collapse with pulmonary edema, and worsen TAH function. The only therapeutic option is to try to restore mechanical function of the device. One liter of normal saline solution should be administered intravenously to treat for possible hypovolemia. Assisted ventilation should be performed as needed, and the patient should be transported to the hospital as soon as possible. Fig. 86.4 provides an algorithm for evaluation and treatment of a patient with a TAH who is altered mentally, unresponsive, or in respiratory distress.
Cardiopulmonary Resuscitation Using a Mechanical Cardiopulmonary Resuscitation Device
Delivering high-quality chest compressions to achieve ROSC and maintain perfusion to vital organs is vitally important to improving survival and neurologic outcome after cardiac arrest. However, manual conventional chest compressions are frequently affected by fatigue, varying skill levels and training, pauses during defibrillation and the switch of rescuers, and adherence to protocols. It is even more difficult to ensure high-quality chest compressions during transport. Studies showed that manual compressions provide only approximately 30% of normal cardiac output, at best. Mechanical chest compression devices have therefore been developed to improve CPR. These devices are designed to deliver compressions of consistent rate and depth, eliminate fatigue as a factor, and provide an opportunity to reduce the frequency and length of pauses in compression.
Initial experimental studies with the mechanical chest compression device showed improved organ perfusion pressures, enhanced cerebral blood flow, and higher end-tidal CO 2 compared with manual CPR. A recent large multicenter randomized controlled trial showed, nevertheless, that an algorithm combining mechanical chest compressions and defibrillation during ongoing compressions provided no survival advantage over manual CPR administered according to guidelines. No difference in survival or neurologic outcome was seen for up to 6 months after the cardiac arrest, even though the mechanical chest compression devices reduced interruptions in chest compressions, and enabled defibrillation during ongoing compressions.
The possible explanation for this discrepancy between early studies and the large clinical trial is that application of the mechanical device resulted in long pauses of chest compression (median device application time 36.0 seconds), and pause in chest compression is clearly associated with worse clinical outcome. Therefore the 2015 AHA Guidelines for CPR and ECC recommended that manual chest compressions remain the standard of care for the treatment of cardiac arrest, but mechanical CPR devices may be a reasonable alternative for use by properly trained personnel in specific settings where the delivery of high-quality manual compressions may be challenging or dangerous for the provider (e.g., limited rescuers available, prolonged CPR, during hypothermic cardiac arrest, during preparation for extracorporeal CPR [ECPR]). Future emphasis should be placed on streamlining and appropriately timing the deployment of these compression devices.
Echocardiography in Cardiac Arrest
For nonshockable rhythms, the essential step will be early detection and correction of potentially reversible underlying causes, such as the Hs and Ts of PEA arrest, as described earlier. Echocardiography has revolutionized our ability to assess the etiology and hence the management of these patients. However, performing and interpreting echocardiography frequently proves much more challenging in the real scene of cardiac arrest.
Point-of-care (POC) focused echocardiography can help assess the volume status, ventricular function, valvular disease, cardiac tamponade, PE, and tension pneumothorax. The TEE, compared with transthoracic echocardiography, provides constant visualization of the heart during chest compressions and gives live feedback on cardiac contractility and the quality of compressions. It is less affected by the body habitus, presence of subcutaneous air, and by chest movements. Several studies have evaluated the feasibility and clinical influence of TEE in cardiac arrest patients. TEE showed moderate sensitivity and specificity for diagnosing cause of arrest, and may further impact treatment. However, it is unclear if these benefits will be translated to improved patient outcome. Thus the 2015 AHA Guidelines for CPR and ECC suggested that if a qualified sonographer is present and use of ultrasound does not interfere with the standard cardiac arrest treatment protocol, then ultrasound may be considered as an adjunct to standard patient evaluation and resuscitation measures.
More recently, POC focused echocardiography has also been used to predict short-term outcome in patients with cardiac arrest. Recent meta-analysis showed spontaneous cardiac movement had a sensitivity of 95% and specificity of 80% to predict ROSC, and sensitivity 90% and specificity 78% to predict survival to hospital admission. Absence of spontaneous cardiac movement on echocardiography has a low likelihood of favorable outcome and can aid in the decision of termination of resuscitation. The caveat is that the interpretation of spontaneous cardiac movement is still very operator-dependent. In addition, in cases of significant bradycardia, the image could be potentially interpreted as cardiac standstill between the cardiac contractions.
Cardiac or Respiratory Arrest Associated With Opioid Overdose
In the United States in 2013, 16,235 people died of prescription opioid toxicity, and an additional 8257 died of heroin overdose. In 2012, opioid overdose became the leading cause of unintentional injurious death in people aged 25 to 60 years in the United States, accounting for more deaths than motor vehicle collisions. A majority of these deaths are associated with prescription opioids. In consideration of this epidemiology, the 2015 AHA Guidelines for CPR and ECC on BLS recommended that for patients with known or suspected opioid addiction who are unresponsive with no normal breathing but a pulse, it is reasonable for appropriately trained lay rescuers and BLS providers, in addition to providing standard BLS care, to administer intramuscular (IM) or intranasal naloxone.
The ideal dose of naloxone is unknown. In the 2010 AHA Guidelines for CPR and ECC, an empiric starting dose of 0.04 to 0.4 mg IV or IM was recommended to avoid provoking severe opioid withdrawal in patients with opioid dependency and to allow for consideration of a range of doses, depending on the clinical scenario. Repeat doses or dose escalation to 2 mg IV or IM was recommended if the initial response was inadequate. Regardless of the care setting and route of administration, the initial goal of therapy is to restore and maintain patent airway and ventilation, preventing respiratory and cardiac arrest, without provoking severe opioid withdrawal.
Recognition and Emergency Response for Suspected Stroke
Each year, about 6.5 million people die from stroke worldwide, and 1 million from cerebrovascular diseases in the 15 countries of the European Union. According to the 2013 Global Burden of Disease study, stroke is the second largest contributor to disability-adjusted life years (113 million disability-adjusted life years) in the world after ischemic heart disease, is a major cause of disability, and is the second most common cause of dementia, after Alzheimer disease. Identifying clinical signs of possible stroke (sudden weakness or numbness of the face, arm, or leg, especially on one side of the body; sudden confusion, trouble speaking, or understanding; sudden trouble seeing in one or both eyes; sudden trouble walking, dizziness, loss of balance, or coordination; or sudden severe headache with no known cause) is important because fibrinolytic treatment must be provided within a few hours of onset of symptoms. Community and professional education is essential to increase the early recognition and treatment to improve patient outcome.
The AHA and American Society of Anesthesiologists developed a community-oriented “stroke chain of survival” that links actions to be taken by patients, family members, and healthcare providers to maximize stroke recovery. Important components of this chain are rapid recognition and reaction to stroke warning signs, rapid EMS dispatch, transport and hospital pre-notification, and rapid diagnosis and treatment in the hospital. The algorithm goals for management of patients with suspected stroke is illustrated in Fig. 86.5 .
Recognition and Management of Specific Arrythmias
This section highlights recommendations for management of patients with acute symptomatic arrhythmias. It needs to be emphasized that electrocardiographic and rhythm information should be interpreted within the context of total patient assessment. For example, when a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient’s condition. Errors in diagnosis and treatment are likely to occur if ACLS providers base their treatment decisions solely on rhythm interpretation and neglect the clinical evaluation of each specific patient.
In general, “unstable arrhythmias” refer to a condition in which vital organ function is acutely impaired due to inefficient cardiac contractions and insufficient cardiac output, or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. “Symptomatic arrhythmias” imply that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases, more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases, the provider must make an assessment as to whether the arrhythmia is causing the patient to be unstable or symptomatic. It is critically important to determine the cause of the patient’s instability in order to properly direct the treatment.
Bradyarrhythmias
Bradycardia is defined as a heart rate of less than 60 beats/min. However, when bradycardia is the cause of symptoms, the rate is generally less than 50 beats/min. A slow heart rate may be physiologically normal for some patients, whereas a heart rate of more than 50 beats/min may be inadequate for others. Hence, 50 beats/min is a relative number, and it is important to also assess the patient’s clinical presentation.
Depending on the origin of the arrhythmia, bradyarrhythmias can be classified as supraventricular (sinus, junctional, or various degrees of atrioventricular [AV] block) or ventricular (complete heart block with a very slow idioventricular escape rhythm). Sinus (or junctional) bradycardia and type I (AV nodal) second-degree block are usually manifestations of increased vagal tone. AV blocks are classified as first, second, and third degree. A first-degree AV block is defined by a prolonged PR interval (>0.20 second) and is generally benign. Second-degree AV block is divided into Mobitz types I and II. In Mobitz type I block, the block is at the AV node and is often transient and asymptomatic. In Mobitz type II block, the block is usually below the AV node within the His-Purkinje system; this block is often symptomatic, with the potential to progress to complete (third-degree) AV block. Third-degree AV block may occur at the AV node, bundle of His, or bundle branches. When third-degree AV block is present, the atria and ventricles are completely dissociated. Third-degree AV block can be permanent or transient, depending on the underlying cause.
Because hypoxemia is a common cause of bradycardia, initial evaluation of any patient with bradycardia should focus on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxygen saturation as determined by pulse oximetry. If oxygenation is inadequate or the patient shows signs of increased work of breathing, supplementary oxygen should be provided. A monitor should be attached to the patient for blood pressure, ECG, and oxygen saturation monitoring, and IV access should be established. If possible, obtain a 12-lead ECG to better define the rhythm. While initiating treatment, evaluate the patient’s clinical status and identify potentially reversible causes.
The provider must identify signs and symptoms of poor perfusion and determine if those signs are likely to be caused by the bradycardia. If the signs and symptoms are not due to bradycardia, the provider should reassess the underlying cause of the patient’s symptoms. Asymptomatic or minimally symptomatic patients do not necessarily require treatment unless there is suspicion that the rhythm is likely to progress to symptoms or more advanced bradyarrhythmias (e.g., Mobitz type II second-degree AV block in the setting of acute myocardial infarction). If the bradycardia is suspected to be the cause of acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock, the patient should receive immediate treatment.
Atropine remains the first-line drug for acute symptomatic bradycardia. The recommended atropine dose for bradycardia is 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg. Doses of atropine sulfate of less than 0.5 mg may result in paradoxical bradycardia. Atropine will also unlikely be effective in patients who had heart transplantation because the transplanted heart lacks vagal innervation. Since atropine works by reversing the muscarinic effects of the parasympathetic nervous system, it is not the preferred drug of choice for type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be more distal than the AV nodes. These bradyarrhythmias are not likely to be responsive to atropine and should be treated with transcutaneous pacing (TCP) or β-adrenergic agonists as temporizing measures while the patient is prepared for transvenous pacing.
If bradycardia is unresponsive to atropine, IV infusion of β-adrenergic agonists (dopamine, epinephrine) can be considered. Dopamine is a catecholamine with both α- and β-adrenergic actions. It can be titrated to more selectively target heart rate or vasoconstriction. At lower doses, dopamine has a more selective effect on inotropy and heart rate; at higher doses (>10 μg/kg/min), it also has vasoconstrictive effects. Epinephrine, as described previously, is a catecholamine with α- and β-adrenergic actions. Isoproterenol is a β-adrenergic agent with β-1 and β-2 effects, resulting in an increase in heart rate and vasodilation. The recommended adult dose is 2 to 10 μg/min by IV infusion, titrated to the appropriate heart rate and rhythm response.
TCP can be done through the multifunctional pacing/defibrillating pads. It is painful, and sedation should be considered in all awake patients. TCP should be considered a temporary measure only, and the patient should always be prepared for transvenous pacing. Expert consultation should be obtained as soon as possible. Transesophageal atrial pacing can be effective in treating intraoperative supraventricular bradyarrhythmias such as sinus or junctional bradycardia. This device is compatible with most external pacing devices and defibrillators. However, transesophageal pacing is only effective at pacing the atria, at least in its current configuration. In a patient who has AV conduction issues, such as complete heart block, this intervention is ineffective. Effective and consistent pacing also relies on normal acid-base status and electrolyte concentrations; thus acidemia and electrolyte abnormalities such as severe hyperkalemia need to be corrected if pacing is not successful.
Fig. 86.6 illustrates the bradyarrhythmias treatment algorithm recommended in the 2015 AHA Guidelines for CPR and ECC.
Tachyarrhythmia
Tachyarrhythmia is defined as an arrhythmia with a rate of more than 100 beats/min, although, as with defining bradycardia, an arrhythmia rate of 150 or more beats/min is more likely to cause clinical symptoms. When encountering patients with tachycardia, efforts should be made to determine whether the tachycardia is the primary cause of the presenting symptoms, or secondary to an underlying condition that is causing both the presenting symptoms and the faster heart rate.
Tachycardia can be classified in several ways, based on the appearance of the QRS complex, heart rate, and regularity. Narrow-complex tachycardias (supraventricular tachycardia [SVT], QRS < 0.12 second) include sinus tachycardia, atrial fibrillation, atrial flutter, AV nodal reentry, accessory pathway–mediated tachycardia, atrial tachycardia (including automatic and reentry forms), multifocal atrial tachycardia, and junctional tachycardia. Wide–QRS-complex tachycardias (QRS ≥ 0.12 second) include VT and VF, SVT with aberrancy, preexcited tachycardias (Wolff-Parkinson-White syndrome), and ventricular-paced rhythms.
Because hypoxemia is a common cause of tachycardia, initial evaluation of any patient with tachycardia, similar to those with bradycardia, should focus on identifying signs of increased work of breathing and oxygen saturation. Patients should be closely monitored and supplemental oxygen provided. A 12-lead ECG better defines the rhythm, but the process should not delay immediate cardioversion if the patient is unstable.
If signs and symptoms persist despite provision of supplementary oxygen and support of airway and ventilation, the provider should assess the patient’s degree of instability and determine if the instability is related to the tachycardia. If the patient demonstrates rate-related cardiovascular compromise with signs and symptoms such as acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock suspected to be due to a tachyarrhythmia, the provider should proceed to immediate synchronized cardioversion, which can terminate tachyarrhythmias by interrupting the underlying reentrant pathway. The recommended initial biphasic energy dose for cardioversion of atrial fibrillation is 120 to 200 J. Cardioversion of atrial flutter and other SVTs generally requires less energy; an initial energy of 50 J to 100 J is often sufficient. If the initial 50 J shock fails, the provider should increase the dose in a stepwise fashion. Monomorphic VT with a pulse responds well to monophasic or biphasic waveform cardioversion (synchronized) shocks at initial energies of 100 J. If a patient has polymorphic VT, treat the rhythm as VF and deliver high-energy unsynchronized shocks (defibrillation doses).
If the patient with tachycardia is stable, then determine if the patient has a narrow-complex or wide-complex tachycardia, whether the rhythm is regular or irregular, and for wide complexes whether the QRS morphology is monomorphic or polymorphic. Therapy is then tailored accordingly. For regular narrow-complex SVT, vagal maneuvers such as carotid massage or Valsalva maneuver are used first to terminate the arrhythmia. If vagal maneuvers are unsuccessful, then adenosine is the drug of choice for terminating organized rapid supraventricular arrhythmias. Adenosine slows sinoatrial and AV nodal conduction and prolongs refractoriness, which is very effective in terminating paroxysmal SVT (PSVT), the most common cause of which is reentry within the AV node. The drug is also used to diagnose the underlying mechanism in tachyarrhythmias of uncertain origin (e.g., atrial fibrillation, atrial flutter) by inducing transient block of AV nodal conduction. If adenosine or vagal maneuvers fail to convert PSVT, PSVT recurs after such treatment, or these treatments disclose a different form of SVT (such as atrial fibrillation or flutter), it is reasonable to use longer-acting AV nodal blocking agents, such as the nondihydropyridine calcium channel blockers (verapamil and diltiazem) or β-blockers.
Treatable causes of VT should always be sought before or during pharmacologic or electrical interventions. Hypoxemia, hypercapnia, hypokalemia or hypomagnesemia (or both), digitalis toxicity, and acid-base derangements are obvious causes for VT and should be quickly evaluated and corrected if present. If antiarrhythmic therapy is pursued, procainamide, amiodarone, or sotalol are recommended. Importantly, only one drug should be administered; a second drug should not be added without expert consultation. Hypotension is common with all three of these medications.
The evaluation and management of tachyarrhythmias is illustrated in the 2015 ACLS Tachycardia with Pulse Algorithm ( Fig. 86.7 ). The medications used for tachyarrhythmia are listed in Tables 86.2 and 86.3 .
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