Chapter 17. Cardiopulmonary Resuscitation

Cardiovascular disease remains the leading cause of death in the United States.1,2 Acute myocardial infarctions associated with ischemic heart disease accounts for the majority of sudden deaths.3

Sudden cardiac death is the unexpected, nontraumatic, abrupt cessation of effective cardiac function associated with absent or acute symptoms of less than 1 hour.4,5 Prodromes such as chest pain, palpitations, or fatigue may occur within the preceding 24 hours.4 The majority of deaths occur within 2 hours of the onset of symptoms.1,2,6–8 Most victims die before reaching a hospital.1,2

Cardiopulmonary resuscitation (CPR) describes the emergency measures used to restore cardiovascular and respiratory function. Notably, cardiocerebral resuscitation represents preferable terminology as it conveys more appropriate emphasis on neurologic recovery. Clinical interventions have been formulated as Advanced Cardiac Life Support (ACLS) guidelines9 based on scientific data established by the American Heart Association (AHA) and International Liaison Committee on Resuscitation.10

CPR and/or ACLS are performed in 1 to 2% of patients admitted to teaching hospitals (including approximately 30% of patients who die).11,12 The goals are to restore spontaneous circulation (ROSC), and ultimately, survive. Early defibrillation is the single most effective means for ROSC. Otherwise, ROSC depends on improving myocardial perfusion and treating underlying disorders. Mechanical circulatory support devices and therapeutic hypothermia represent treatment interventions that may improve these life-saving endeavors. Overall survival rates remain low (Table 17-1), and successful resuscitation frequently results in neurologic impairment.13–15,129 The clinical integration of rapid response, early defibrillation, circulatory support devices, hypothermia, and neuroprotective agents should improve future outcomes.

Peripheral venous access is preferred for speed, and avoiding CPR interruption. Drugs take 1 to 2 minutes to reach the central circulation during CPR. Administration should be by bolus followed by flushes and extremity elevation. Peak drug concentrations are lower with peripheral versus central injection. Central access should be considered when responses to peripheral administration are absent. Internal jugular and supraclavicular sites are preferred to the femoral because return to the inferior vena cava is impaired during CPR. Long femoral lines may overcome this problem. Routine fluid administration is not indicated without evidence of hypovolemia as this may adversely affect coronary pressure by raising right atrial pressure.

When venous access is not possible, drugs may be administered via an endotracheal tube. Medications are given via a catheter passed beyond the tube's tip using twice the IV dose diluted in saline or water. Water provides better absorption but results in more adverse effects on Pao2. Rapid insufflations are given after each bolus for drug dispersion. Intracardiac injection is not recommended during routine CPR. It may be used for epinephrine during open chest cardiac massage (OCM), or if no other access is obtainable. Intracardiac injection can result in complications including: cardiac injury, tamponade, and pneumothorax.

The principal agents recommended for ACLS are adrenergic agonists and antiarrhythmics. Alpha-adrenergic agonists have been the only drugs that definitively improved outcome in CPR. Their primary benefit is vasoconstriction. Increased peripheral resistance results in elevated aortic pressure, improving coronary perfusion. The minimum coronary perfusion pressure and blood flow needed for successful defibrillation are 15 mm Hg and 15 to 20 mL/min/100 g, respectively. CPR rarely achieves these minimums without pressors. Epinephrine has this beneficial effect. Its beta-adrenergic effect may improve the treatment of cardiac arrest. One milligram is recommended every 3 to 5 minutes during resuscitation attempts.10 Epinephrine improves ROSC and survival in animal models of cardiac arrest. Clinical trials using higher epinephrine doses demonstrated higher rates of ROSC, but no survival advantage.16,17 One trial found high-dose epinephrine had more adverse effects, which may be partly explained by increased oxygen demands.

Other nonadrenergic vasoconstrictive agents have been studied as alternatives to epinephrine. Vasopressin acts on unique receptors and may be beneficial for treating cardiac arrest refractory to epinephrine. Laboratory and clinical data indicate vasopressin may be preferable to epinephrine.18,19 A recent meta-analyses of five randomized clinical trials comparing vasopressin to epinephrine during cardiac arrest20 found no evidence to support the use of one drug over the other. Epinephrine is less expensive. However, vasopressin continues to be an acceptable alternative for treating cardiac arrest.

Vasopressin also mediates adrenocorticotropin release during CPR.21 The hypothalamic-pituitary-adrenal axis is suppressed in cardiac arrest victims,21–23 and low serum cortisol levels have been identified as a poor prognostic factor for ROSC.22,23 Adrenal function in patients who have ROSC may also be insufficient for survival.24 Further clinical trials are needed to determine if administration of corticosteroids during CPR and/or following ROSC may benefit outcome.

The effectiveness of antiarrhythmics in sudden death has not been well substantiated. Randomized clinical trials have demonstrated amiodarone effectiveness in treating cardiac arrest.25–29 Amiodarone significantly improved survival to hospital admission compared with placebo for VF/VT.28 The most recent randomized clinical trial found amiodarone significantly increased survival to hospital admission compared to lidocaine when used to treat sudden death.25 Survival to discharge was observed, but did not reach statistical significance. Amiodarone is recommended for the treatment of persistent VT and/or VF. Lidocaine is an acceptable alternative.

Magnesium sulfate should be administered for suspected hypomagnesemia or torsades de pointes. It is recommended for refractory VF/VT. Hypomagnesemia is associated with ventricular arrhythmias and sudden cardiac death and may hinder potassium replenishment in hypokalemic patients. Hypermagnesemia can cause flaccid paralysis and cardiorespiratory arrest.

Atropine enhances atrioventricular node conduction and sinus node automaticity. It is indicated for symptomatic bradycardia and asystolic arrest. Asystole from prolonged ischemia is usually fatal. Atropine is unlikely to benefit, but is not harmful in such circumstances. Adverse effects include tachycardia and anticholinergic effects.

Judicious use of NaHCO3 may be appropriate for correcting severe acidosis during cardiac arrest. Notably, NaHCO3 increases CO2, which may accumulate rapidly, leading to a hypercarbic venous acidemia. Diffusion of CO2 across cell membranes may result in paradoxic intracellular acidosis and decrease the likelihood of successful resuscitation. Hypocarbic arterial alkalemia or the so-called venoarterial paradox may develop. Therefore, NaHCO3 may increase CO2 levels, worsen the venoarterial paradox, and exacerbate intracellular acidosis. Other potential adverse effects include alkalemia with leftward shifts in the oxyhemoglobin desaturation curve, hyperosmolality, hypernatremia, and hypotension. Finally, NaHCO3 has not been shown to improve results in cardiac arrest and is only recommended for severe acidosis, hyperkalemia, tricyclic antidepressant overdose, or prolonged CPR.9

Basic life support (BLS) defines the methods used to sustain ventilation and blood flow until ACLS can restore spontaneous circulation. Airway, breathing, circulation, defibrillation (ABCD) algorithms describe these standardized approaches (Fig. 17-1).3

Airway Management

Initial management of unresponsive patients is ensuring a patent airway.9 The airway is open using the head-tilt–chin-lift maneuver. The jaw-thrust technique is an alternative for suspected neck trauma; however, it is more difficult to perform. Both relieve posterior displacement of the tongue, which is a common cause of airway obstruction. Difficult ventilation should be addressed by repositioning and considering foreign body obstruction. The Heimlich maneuver, or subdiaphragmatic abdominal thrust, is recommended for relieving obstruction from foreign bodies. Rapid thrusts to the subxiphoid region can dislodge a foreign body by increasing expiratory pressure. Chest thrusts are more appropriate for obese patients and women in late stages of pregnancy. Magill forceps can be used to retrieve foreign bodies when necessary.

Masks, and oral and nasal airways may be used with mouth-to-mask ventilation or bag-valve devices. Bag-valve devices reduce exposure to potential infection, but require two rescuers.10 Nasopharyngeal airways are considered for nonintubated patients. Oropharyngeal airways can be used in unconscious patients but add risk for laryngospasm and regurgitation.10

Endotracheal intubation (ETT) is the preferred method of airway management. ETT maintains an open airway, decreases risk of gastric distention and aspiration, and is an alternative drug administration route. Orotracheal intubation is ideal unless a neck injury is suspected, in which case nasotracheal intubation is recommended. ETT can be complicated by esophageal intubation, oral trauma, pharyngeal laceration, vocal cord injury, pharyngeal-esophageal perforation, mainstem bronchus intubation, and aspiration. Esophageal intubation is likely with a low end-tidal CO2 (ETCO2).

Transtracheal catheter ventilation (TTC) can be instituted when routine methods fail using a catheter passed across the cricothyroid membrane. TTC may cause suboptimal ventilation, including pneumothorax, hemorrhage, and esophageal perforation. Cricothyroidotomy may also be considered for difficult airways. Otherwise, tracheostomy is indicated when ventilation cannot be achieved.

Mouth-to-mouth ventilation/nasal is used in the absence of airway devices and generally results in adequate ventilation. Respiratory rates of 10 to 12 per minute are recommended.10 Cricoid pressure (Sellick maneuver), maintaining a patent airway, and slow breaths decrease risk for gastric distention, regurgitation, and aspiration. Concern of transmissible diseases during resuscitation has reduced enthusiasm for CPR. Barrier devices (face shields and masks) have been developed to protect from exposure. Chest compressions alone are better than no resuscitation attempt. Interestingly, there is increasing evidence that chest compressions alone may result in survival rates and neurologic outcomes comparable to CPR with ventilation.29,30,128

Closed Chest Cardiac Massage

Closed chest cardiac massage (CCM) is the principal means of restoring blood flow during CPR. CCM is best when the victim is supine on a firm surface (Fig. 17-2). Compressions are given to the lower sternum at 100/min, with a rate of 30 compressions: 2 breaths. Compressions of 4 to 6 cm should occupy 50% of the cycle. At best, CCM creates minimal perfusion to vital organs and is unable to sustain life.31–34 Survival becomes exceedingly low with more than 30 minutes of CCM. ROSC is dependent on proper CCM techniques,33 but studies have demonstrated these techniques are frequently suboptimal.31,32

Discontinuation of CPR

Discontinuation of CPR remains controversial, with no clearly defined criteria. Determining the adequacy of CCM is subjective because palpable pulses do not signify forward flow. Reactive pupils and/or spontaneous respirations indicate some cerebral perfusion, but correlate poorly with outcome. Aortic diastolic pressure may be the best measure of CPR effectiveness35 but is usually not available.

Alternatively, ETCO2 can provide useful information and predict ROSC.36,37 Low ETCO2 suggests poor perfusion, esophageal intubation, airway obstruction, massive pulmonary embolus, or hypothermia.

Successful ROSC and survival are influenced by many factors. Ventricular fibrillation (VF), early defibrillation, rapid onset of CPR or ACLS, witnessed arrest, and early age all have favorable implications.38,39–41,42 These factors, should all be considered before abandoning resuscitation.

Complications of CPR

Common complications associated with CCM are rib and sternal fractures.43 Others include aspiration, gastric dilatation, anterior mediastinal hemorrhage, epicardial hematoma, hemopericardium, myocardial contusion, pneumothorax, air embolus, hemothorax, lung contusion, and oral/dental injuries.43–45 The liver and spleen are the most commonly injured intra-abdominal organs, reported in 1 to 2% of cases.43 Significant injuries can involve the trachea, esophagus, stomach, cervical spine, vena cava, retroperitoneum, and myocardium.43

Sudden death generally presents as ventricular fibrillation/tachycardia (VF/VT), asystole, or electromechanical dissociation (EMD), also called pulseless electrical activity (PEA). VF may continue after defibrillation attempts (shock-resistant) or persist despite other therapeutic interventions (persistent or refractory). Also, successfully treated VF may recur (recurrent). These patterns are felt to have different etiologies, priorities of treatment, and prognoses. Early identification of the underlying rhythm is important for selecting the recommended treatment algorithm (see Fig. 17-1).

Ventricular Tachycardia

Ventricular tachycardia (VT) is an arrhythmia characterized by premature ventricular depolarizations (>100/min). Cardiac arrest occurs with rapid, sustained VT. VF is uncoordinated, continuous contraction of the ventricles. More than 80% of monitored cardiac arrests originate with VF/VT.46 Most survivors have VF/VT as the initial rhythm.38,41,47 Rapid defibrillation is the key determinant for survival38,48,49 and should precede all other therapy if immediately available.9,10 Delay negatively impacts successful defibrillation.50 Mortality increases 4 to 10% for every minute preceding defibrillation attempts.48 Survival rates approach zero when countershocks are attempted more than 10 to 12 minutes after arrest.51 Current guidelines therefore emphasize early defibrillation and use of automated external defibrillation systems.10

Optimal treatment VF or pulseless VT begins with immediate defibrillation, when possible. Energy for initial defibrillation is 200 J. If VF continues, a second shock (200 to 300 J) is given immediately. A third countershock (360 J) is given if the second fails. It is vital that three consecutive shocks are given without delay for other interventions. CPR is performed whenever defibrillation attempts fail. Figure 17-3 outlines treatment algorithms for persistent VF/VT. Epinephrine or vasopressin is given IV or via the endotracheal tube. Vasopressin should only be given once, and subsequent defibrillation attempted (360 J). Epinephrine is given every 3 to 5 minutes. Refractory VF is treated with antiarrhythmics. Amiodarone may be the most efficacious in this setting.25–27,52 Lidocaine is also acceptable for recurrent VF or pulseless VT; however, it is not recommended over amiodarone.38 Defibrillation should be attempted 30 to 60 seconds after each drug.10

Prognosis for VF or pulseless VT is better than for asystole or PEA. Up to 30% of patients with witnessed VF/VT arrest are successfully resuscitated.41,47,53,54 Failure of initial defibrillation attempts is a poor prognostic sign.

Asystole

Asystole is absence of electrical and mechanical cardiac activity and frequently indicates a terminal event. ACLS is indicated while other treatable causes are considered. Priorities include effective CPR and rhythm confirmation. Low-amplitude VF may occasionally masquerade as asystole. Incorrect lead placement or equipment malfunction should be considered. Countershocks do not benefit true asystole, and may induce parasympathetic discharge diminishing the chance of ROSC.

Once verified, asystole is managed by ABCD guidelines. Epinephrine raises perfusion pressures10 and is repeated every 3 to 5 minutes. Atropine treats the high parasympathetic tone underlying severe brady-asystolic arrests. Transcutaneous or transvenous pacing may be effective if applied early. Timely pacing can result in successful capture and effective cardiac contraction.55 The prognosis of asystole is grim, but may be better when preceded by VF versus prolonged CPR.

Pulseless Electrical Activity

Pulseless electrical activity generally carries a very poor prognosis. Characterized by organized electrical activity without effective cardiac contractions, PEA is synonymous with EMD and includes pulseless idioventricular, bradycardia, and ventricular escape rhythms.10 These dysrhythmias are common proximate causes of death in delayed or difficult resuscitations. As with asystole, PEA mandates assessment for reversible causes. Rapid, narrow-complex activity may indicate a treatable condition. Associated trauma may be an indication for emergency thoracotomy56 to address cardiac tamponade of cardiovascular injury. Thoracotomy allows cardiac massage and aortic occlusion, which may be lifesaving. PEA following open heart surgery is a clinical scenario in which chest reopening is generally recommended.57

Cardioversion

Cardioversion is the only effective treatment for VF. Defibrillation depolarizes and results in temporary asystole.58 Pacemaker cells then restore myocardial activation. Myocardial contraction resumes if high-energy phosphates depleted by CPR are sufficient. The probability of successful defibrillation is best immediately after witnessed arrests. Success rates decline rapidly during CPR, which only slows the deteriorating state. Once available, a defibrillator should be positioned with quick-look paddles for rhythm evaluation. VF or pulseless VT is treated immediately. Blind defibrillation is rarely indicated. Asynchronous shocks are given for VF or pulseless VT. Synchronous shocks are given for stable rhythms (eg, atrial fib/flutter, monomorphic VT)10 to avoid impinging on the relative refractory period.

Energy levels for cardioversion impact success. Low currents may be ineffective and excessive energy levels cause myocardial injury.59,60 The lowest energy for defibrillation is desired. A prospective study demonstrated that 175 and 320 J were equally effective for initial defibrillation attempts;61 therefore, 200 J is recommended for initial defibrillation attempts.10 The range for second countershocks is 200 to 360 J.

Body size impacts defibrillation energy requirements.10 The optimal current for defibrillation is 30 to 40 A.62 Adult transthoracic impedance is 70 to 80 gV, requiring a 200-J countershock for a 30-A current.63 However, impedance varies significantly depending on energy delivery, chest size, electrode size, interelectrode distance, paddle-skin coupling, respiration, and antecedent countershocks.62 Keep one electrode positioned on the right parasternal border below the clavicle, and the other in the left midaxillary line, level with the nipple.10 Electrodes must not touch so the currents pass through the heart. During open chest resuscitation, one paddle is placed over the right ventricle, and the other behind the apex. Larger paddles are preferred for their lower resistance. Small paddles should only be used if required to fit in the chest.64 It is also noteworthy that compression of the heart reduces the defibrillation threshold.65

Defibrillation threshold (DFT) describes the amount of current required to defibrillate the heart. DFT increases during CPR and is primarily affected by coronary perfusion pressure. Catecholamines decrease the DFT.66 It was thought epinephrine decreased the DFT through beta-adrenergic effects; instead, this is owing to alpha-adrenergic increases in systemic pressure. Time-dependent increases in DFT observed during CPR are not completely understood. Adenosine may act through A1 receptors to increase DFT over time.67 Aminophylline, an adenosine receptor antagonist, decreases DFTs.

The presence of pacemakers and automatic internal cardio defibrillators (AICDs) impact defibrillation management. Paddles should not be placed directly over pacemaker generators,68 and these devices should be interrogated to reassess pacing thresholds after defibrillation. AICDs are not a contraindication to external defibrillation for VF/VT,130 and are shielded to withstand countershocks. AICD patches may increase transthoracic resistance.69 Therefore, paddle orientation should be changed if initial countershocks fail. After defibrillation, the AICD unit should be tested.

Automated external defibrillators (AED) are increasingly common. AEDs analyze ECG pattern, sounds an alarm and discharges when VF is detected. They require less training and are more rapid at administering countershocks.51 AEDs have equivalent survival compared with manual defibrillators.70 Clinical trials have confirmed AEDs can be used safely and effectively by the lay person.71

Current-controlled defibrillators may improve the success of defibrillation.72 These devices enhance delivery of energy and reduce risk of excessive energy delivery. The delivery of biphasic (bidirectional) or multipulse, multipathway shocks are methods used for internal defibrillators,63 but efficacy for external defibrillation has not been established.73

A precordial thump may achieve defibrillation and be used when a defibrillator is not immediately available. It may be successful in 11 to 25% during VT. Unfortunately, precordial thumps may result in VF, asystole, or EMD, and are less unlikely to convert VF.74

Chest compressions must be temporarily discontinued to avoid electrical shock of those performing CPR. This hands-off interval is also used for rhythm analysis before defibrillation. Prolonging the hands-off period can significantly reduce the probability of successful cardioversion, and be kept as short as possible.74

Mechanisms generating forward blood flow during CPR have been a subject of significant controversy. Investigations have demonstrated chest compressions translate directly to the heart.75 However, other mechanisms have been elucidated.

At least two other mechanisms appear responsible for blood flow during CPR. The thoracic pump was discovered by observing that coughing during cardiac arrest generated forward flow. Chest compressions also cause a rise in thoracic pressures capable of forcing blood into the systemic circulation.34 The heart in this circumstance merely functions as a conduit. Many studies have validated the thoracic pump mechanism during CPR.31,76

Another mechanism for blood flow generated during CPR is the abdominal pump. This emphasizes effects of abdominal compressions, which are now advocated for CPR.77 The abdominal pump operates through arterial and venous components. The arterial component reflects compression of the abdominal aorta, forcing blood into the peripheral circulation. The aortic valve remains closed during abdominal compression and resists retrograde arterial flow. Simultaneously, the venous component fills the heart from venous pressure. Both contribute hemodynamic benefits during abdominal compressions in CPR.

Clearly, the cardiac, thoracic, and abdominal pump mechanisms are important concepts of CPR physiology. The technique(s) employed during CPR dictates which mechanism predominates. Other factors that can influence effectiveness of these pump mechanisms include: cycle rates, compression durations, body habitus, cardiac size, chest wall stiffness, and the presence of pulmonary disease, as well as the duration of the resuscitation effort. Understanding these mechanisms has led to improved CPR techniques and adjunctive devices, which are directed towards improved vital organ perfusion.

The high mortality rates associated with cardiac arrest are in part attributed to inadequate perfusion generated by CCM. Therefore a number of adjunctive devices have been developed to enhance the effectiveness of CCM.

Active Compression-Decompression

Active compression-decompression (ACD) is one means for improving the effectiveness of CCM. Originating from successful resuscitation with a plunger, a device consisting of a hand-held suction cup with a central piston was developed (Fig. 17-4). ACD-CPR can increase aortic pressures resulting in improved cerebral, coronary, and renal blood flow.78 Ventricular filling and venous return are augmented by negative intrathoracic pressure during the active decompression phase. Two studies reported increased ROSC and 24-hour survival with the ACD device. Survival to discharge was higher with ACD in both studies but did not reach statistical significance.79,80 Data from 2866 patients using the ACD device were subsequently combined.81 ACD improved 1-hour survival, but long-term outcome was not significantly different from standard CPR. A randomized clinical trial demonstrated significantly improved 1-year survival following ACD compared with standard CPR.82 Notably, a prospective trial found that combining ACD with controlled ventilation using an inspiratory impedance threshold device improved short-term survival when compared with standard CPR.83

Synchronizing chest and abdominal pumping techniques within the same compression cycle is another means for improving the effectiveness of CCM. Termed, “phased thoracic abdominal compression-decompression CPR” (PTACD-CPR), this technique employs abdominal compression during the relaxation phase of chest compression. Simplified applications involve compressing the chest and abdomen at equal durations. Initial clinical studies using PTACD-CPR yielded improvements in outcome measures.84 Return of spontaneous circulation and survival to discharge were both significantly improved using PTACD-CPR for inpatient cardiac arrests.84–86 A hand-held device has been developed that allows single rescuer PTACD-CPR combined with compression-decompression mechanics (Fig. 17-5). The method was deemed safe and effective by investigators.54 Further studies are warranted to determine its potential impact on survival rates.

Noninvasive Mechanical Devices

Noninvasive mechanical devices have been developed to enhance the ergonomics of CPR. These devices assist in improving CPRs performance effectiveness, which can minimize the fatigue associated with performing CPR.

Fatigue becomes a particularly significant problem when attempting to perform ACD-CPR for extended periods of time. This led to developing an automatic chest compression device. Clinical applications have found its use feasible for out-of-hospital CPR.87 Preliminary trials indicated the device improves the 30-day survival of patients suffering witnessed cardiac arrest.88

The pneumatic vest is another noninvasive mechanical device that alternates pressures around the thoracic cage (Vest-CPR). Vest-CPR utilizes a pneumatic bladder tailored to fit the chest wall. Air is forced into and out of the vest by a pneumatic drive. Clinical trials demonstrated improved outcomes with an increased rate of ROSC.89 Another device has been described that employs a constricting band.90 This portable device is currently available that provides mechanical vest-CPR (Fig. 17-6). Further trials are needed to determine the impact of vest-CPR devices on clinical outcomes.

Open Chest Cardiac Massage

Open chest cardiac massage is a valuable resuscitative method that is effective at returning blood flow during cardiac arrest. OCM was popularized by surgeons for resuscitation before 1960. The technique is currently advocated for specific circumstances such as cardiac arrest from penetrating chest trauma. Precluding effective CPR, OCM should also be considered for cardiac arrest resulting from hypothermia, massive pulmonary embolism, pericardial tamponade, intrathoracic hemorrhage, postcardiotomy arrest, and chest deformity. OCM is usually performed via a left lateral thoracotomy except after recent cardiac surgery for which the prior sternotomy is reentered. A left thoracotomy is performed at approximately the fifth intercostal space. The pericardium is entered anterior to the phrenic nerve and the heart compressed between both hands. Alternatively, one-hand massage may be performed while using the other to control bleeding or occlude the descending thoracic aorta (Fig. 17-7).

Numerous studies have demonstrated superior hemodynamics during OCM compared with CCM.91,92 Notable are increased diastolic pressures and reduced central venous pressures,57 which favorably impacts coronary perfusion compared with CCM. Cardiac output and cerebral blood flow are higher during OCM,92 explaining how OCM can successfully ROSC after failed efforts with CCM. However, outcomes cannot be expected to improve when OCM follows prolonged CPR.93 Laboratory studies suggest that OCM can improve outcomes if applied after relatively short durations of ineffective CCM. A prospective, nonrandomized clinical trial illustrated the importance of instituting OCM earlier to improve outcome.94 Patients who received OCM had improved outcomes, which declined as the duration of CCM before OCM increased.

Timely application of OCM can improve survival in a variety of clinical scenarios. One setting in which OCM has been used routinely is in the postcardiotomy ICU. One review strongly confirmed the benefit of open chest massage in patients suffering cardiac arrest following open heart surgery.57 The study found that reopening the chest in this setting has the greatest potential benefit in patients arresting within 24 hours of surgery and performed within 10 minutes of cardiac arrest.

Potential complications of OCM include right ventricular perforation, hemorrhage, lung laceration, phrenic nerve injury, esophageal and aortic injury, cardiac lacerations, and empyema. Infection is surprisingly low (5%) given the nature of the procedure, and related limitations on sterile technique.

The intra-aortic balloon pump improves hemodynamics during CPR. However, its value in this setting appears limited.

Cardiopulmonary Bypass

Cardiopulmonary bypass (CPB) has seen increased use for treating refractory cardiac arrest.95 Hemodynamics, survival, and neurologic function are improved in experimental models of cardiac arrest treated with CPB versus standard CCM. Although clinical reports are uncontrolled, and frequently anecdotal, the growing body of evidence demonstrates CPB is efficacious for the treatment of not only cardiogenic shock,131 but also cardiac arrest. It is noteworthy that several studies have demonstrated improved survival with good neurologic outcomes using CPB after prolonged periods of CPR. CPR efforts and patient selection are important considerations when interpreting these clinical results. Patients have been successfully bridged to transplantation utilizing CPB after cardiac arrest.96–98 Most impressive are the improved outcomes when CPB was used to treat refractory cardiac arrest.95,132,148 Because of the heterogeneity among these studies, it is difficult to arrive at objective selection criteria. There is also a paucity of reported complications. Therefore, future studies need to better define patient selection criteria and related risk/benefit considerations to guide CPB use (Table 17-2). Prognostic factors that are felt to be important include age, treatable conditions, adequacy of CPR, and timely intervention. Generally, CPB should be instituted within 30 to 45 minutes of witnessed arrests after more extended periods of CCM has been documented.97,99 Clearly, CPB can result in successful resuscitation following prolonged periods of CPR in pediatric cases100,101 and hypothermic cardiac arrests.

Hypothermic cardiac arrest is a unique category in which survival can follow prolonged cardiac arrest. CPB has a unique capability for rewarming during resuscitative circulatory support.102,103 The largest experience in adults treated for hypothermia was reported from Finland.104 Findings indicated that age and arterial pH at presentation had significant prognostic implications. The duration of CPR did not affect the likelihood of survival in these cases.

Direct Mechanical Ventricular Actuation

Direct mechanical ventricular actuation (DMVA) is a unique non–blood contacting device that provides systolic and diastolic actuation of the ventricular myocardium (Fig. 17-8). DMVA is pneumatically regulated with an atraumatic vacuum attachment. Rapid application is performed within minutes through a thoracotomy or sternotomy, which results in physiologic, pulsatile blood flow.105,133 Pulsatile reperfusion probably best explains the improved neurologic outcome following resuscitative circulatory support using DMVA versus CPB in animals.106–108 Lack of blood contact also circumvents the need for anticoagulants and reduces thromboembolic complications. DMVA has been used successfully in humans for bridge to transplantation, postcardiotomy support, and recovery from severe myocarditis.105,134 Recent studies have demonstrated DMVA's favorable effect on maladaptive cell signaling when supporting the severely failing heart.109,110 Myocardial strain analysis has demonstrated myocardial function improves within 10 minutes of DMVA resuscitative circulatory support.111 Particularly notable are the findings of improved neurologic function following resuscitative support with DMVA versus CPB. DMVA's unique ability to provide immediate pulsatile reperfusion may best explain its beneficial impact on cerebral resuscitation.

The goal of CPR is to provide sufficient blood flow to vital organs until definitive intervention. The brain is the organ most vulnerable to ischemia during cardiac arrest. Consciousness is lost in seconds, high-energy phosphates and glycogen stores are depleted in minutes with lactic acid accumulation causing secondary cytotoxic effects. Limited cerebral blood flow actually may exacerbate the sequelae by allowing anaerobic metabolism. These circumstances help explain why CPR out-of-hospital cardiac arrest results in so few neurologically intact survivors.112

Given the importance of cerebral resuscitation, it has been suggested that current CPR protocols put too much emphasis on ventilation. Cardiocerebral resuscitation appears to convey more appropriate emphasis on the brain and fosters the development of new treatment paradigms.113 Recent examples include recommended techniques when performing basic CPR. The reluctance to perform mouth-to-mouth ventilation has led to guidelines for cardiac only resuscitation (chest compressions only). Data from multicenter trials have found cardiac only resuscitation may lead to improved survival and neurologic outcome.30 The findings are best explained by improvements in cerebral blood flow. Specifically, chest compressions are used to initiate CPR and are not interrupted for ventilation.

CCM generates limited blood flow. During CPR, only venous valves can prevent transmission of high, intrathoracic pressures to the jugular venous system. Cerebral blood flow is kept at 50 mL/min/100 g by autoregulation when cerebral perfusion pressures are in the normal physiologic range.114 CPR results in low cerebral perfusion pressures, seldom exceeding 40 mm Hg.115 Cerebral flow is only 10 to 15% of normal, which may be more harmful than no flow at all.

Mechanical circulatory support is an obvious means for improving cerebral blood flow during CPR. This is supported by the growing body of clinical evidence indicating the implementation of CPB after failed CPR attempts improves outcomes. Laboratory investigations have demonstrated pulsatile flow is superior to nonpulsatile flow with regard to cerebral resuscitation. Pulsatile reperfusion results in favorable flow to the gray matter,106 which correlates with increased postresuscitation cerebral high energy phosphate content.107 Cerebral function and histopathology are significantly improved following pulsatile versus nonpulsatile reperfusion.108,135

There are other critical aspects related to cerebral resuscitation, which deserve further consideration. Neurons function for up to 60 minutes during ischemia. However, reperfusion can cause neuronal damage that is multifactorial in origin. Calcium overload, free-radical injury, and no-reflow phenomenon may all contribute to reperfusion injury.114 No-reflow describes states of hypoperfusion that follow cerebral ischemia. Platelet aggregation, altered calcium flux, vasoconstriction, and pericapillary edema are all presumed causative factors. Intracranial pressure may not be as important because it commonly returns to normal after cardiac arrest except after cerebral trauma. Cerebral blood flow remains depressed for 18 to 24 hours after a severe ischemic insult. Subsequent hypoperfusion is believed secondary to calcium-induced precapillary vasoconstriction.

Cerebral blood flow after ischemic injury is critically dependent on perfusion pressure. Moderate hypotension can further cerebral ischemia and injury. Blood pressure should be normal or mildly elevated in the post-resuscitation period. Moderate hyperoxia (PO2 = 100 mm Hg) and mild hyperventilation (Paco2 = 30 to 35 mm Hg) are desirable. Arterial pH is kept in the normal range. Anticonvulsants are given as needed, because seizures are not uncommon after ischemic brain injury.

One of the most significant advances in cerebral resuscitation has been the implementation of therapeutic hypothermia. Mild hypothermia decreases mortality and improves neurologic recovery after cardiac arrest. Two randomized, controlled, clinical trials116,117 confirmed this association. This led to new AHA recommendations for therapeutic hypothermia.118 The subsequent meta-analysis qualified these recommendations.119 More recently, observational studies from growing clinical databases have found the safety and efficacy of hypothermia can be extended to routine clinical practice.120,121 A new clinical device is now available to selectively chill the brain using intra-nasal cooling (Fig. 17-9). Further trials will be needed to demonstrate its effectiveness.

Other considerations after ROSC include continuous hemodynamic monitoring, and use of supplemental oxygen. Antiarrhythmics are continued as arrhythmias commonly occur from increased circulating catecholamines. Beta-adrenergic blockade should be instituted, unless bradycardia is a problem. Bradycardia requires airway and ventilation be carefully assessed. Atropine, epinephrine, and/or pacing are indicated if hypotension accompanies bradyarrhythias.

Antiarrhythmics, pacemakers, and automatic internal cardiodefibrillators are also important considerations for patients surviving sudden death. Clinical studies have shown survival can be significantly improved with these interventions.72,122,123 Amiodarone has also been shown to be effective in this regard.

Predicting which patients will survive resuscitation efforts remains elusive. Patients presenting in VF/VT have a better prognosis compared with asystole or PEA.11,41,47 Advanced age may not be a prognostic indicator when considering other comorbidities.11,12,42,47 Location of the arrest (ICU versus non-ICU) also impacts outcome.11,12 Comorbid conditions are associated with more than 95% of mortalities after cardiac arrest including renal failure, metastatic cancer, pneumonia, sepsis, hypotension, stroke, and homebound lifestyle.11 Survival is more likely for witnessed arrests, early defibrillation CPR initiated within 5 minutes, CPR durations less than 15 minutes, and postresuscitation hypothermia is implemented. Mortality increases from 44% for CPR less than 15 minutes to 95% for CPR that is longer in duration.11,42

In contrast to inpatients, where comorbidities play a major role, delayed therapy outweighs all other prognostic factors for out-of-hospital arrests. Other key determinants for survival include the initial rhythm, witnessed arrest, downtime before CPR, and any delay in treatment. Early definitive care is associated with improved outcome. As with in-hospital arrest, VF/VT has the best prognosis, and bystander CPR is strongly associated with improved survival rates.118 Decreased mortality from bystander CPR is primarily from reduced postresuscitation anoxic encephalopathy. Return of consciousness within 24 to 48 hours of arrest is a favorable prognostic sign.11 Therapeutic hypothermia has significantly enhanced the likelihood of neurologic recovery and survival.

Long-term survival in patients discharged after an out-of-hospital arrest is very reasonable. Reported 1-year survival rate ranges from 75 to 85%, and approximately 50% are still alive at four years (see Table 17-1). The majority of these patients ultimately die of cardiac causes.14,124 Positive predictors for long-term survival are: cardiac arrest associated with acute myocardial infarction (MI), no prior history of MI, and also short-time intervals between arrest, CPR, and definitive care.125 Primary antiarrhythmic events, congestive heart failure, impaired left ventricular function, extensive coronary artery disease, and complex premature ventricular depolarizations are less likely to result in long-term survival after discharge.

Unfortunately, not all patients who survive sudden death have a subsequent good quality of life.126 Depression is a common problem following discharge, but usually resolves within a few months.11 The incidence and characteristics of mental impairment in those who survive is variable. Significant neurologic impairment usually results in death before hospital discharge. While neurologic deficits can be very disabling,127,134 many survivors of sudden death retain normal neurologic function.

Resuscitation efforts should be discontinued when ACLS efforts do not result in ROSC. Discontinuation is based on clinical judgment. Although several studies have shown that CPR for longer than 30 minutes is unlikely to result in long-term survival. There are many growing reports of neurologically intact survivors after prolonged resuscitation.11 This is particularly evident when examining the use of mechanical circulatory support. Considerations for discontinuing ACLS should also include underlying medical conditions.

Early defibrillation, effective BLS, and timely ACLS measures represent the major theme in the treatment of cardiac arrest. Unfortunately, survival rates have remained disappointingly low. A more appropriate focus on cerebral resuscitation should substantially improve future clinical outcomes. The use of circulatory support in patients that fail initial ACLS efforts has clearly demonstrated promise when initial resuscitation efforts fail. Defining qualified selection criteria and treatment protocols will require further study. Additionally, it will be important to implement those therapies that improve neurologic recovery. Therapeutic hypothermia has clearly had one of the greatest recent impacts in this regard. Integrating hypothermia, resuscitative circulatory support devices, and cerebroprotective agents has compelling potential. They can justify and help guide future clinical trials. New paradigms and treatment protocols for CPR may evolve from these critically needed investigations.