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Anstadt MP, Lowe JE. Cardiopulmonary Resuscitation.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:471494.

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Chapter 16

Cardiopulmonary Resuscitation

Mark P. Anstadt/ James E. Lowe

TECHNIQUES IN CARDIOPULMONARY RESUSCITATION
????Airway Management
????Closed Chest Cardiac Massage
????Discontinuation of CPR
????Complications of CPR
SUDDEN DEATH TREATMENT CONSIDERATIONS
????Ventricular Tachycardia
????Asystole
????Pulseless Electrical Activity
????Cardioversion
PHYSIOLOGY OF CARDIOPULMONARY RESUSCITATION
CPR TECHNIQUES AND MECHANICAL ADJUNCTS
????Noninvasive Mechanical Devices
????Active Compression-Decompression
????Open Chest Cardiac Massage
????Blood Pumps
????Direct Mechanical Ventricular Actuation
PHARMACOLOGIC THERAPY DURING CPR
CEREBRAL PROTECTION/RESUSCITATION
ETHICAL CONSIDERATIONS
CONCLUSION
REFERENCES

?? INTRODUCTION
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Cardiovascular disease remains the leading cause of death in the United States. Over 6 million people in the United States have significant coronary artery disease (CAD).1 In 1991 an estimated 478,000 deaths were due to coronary artery disease.1 Nearly a third occurred in persons less than 65 years of age.1 While death rates from cardiovascular disease decreased 25.7% between 1981 and 1991, the actual number of deaths decreased only 6% due to the aging population.1,2 More recently it has been estimated that 900,000 acute myocardial infarctions occur annually in the United States.3 Of the 225,000 deaths, 125,000 occur in the field, which accounts for the majority of sudden cardiac deaths in the United States.3

Sudden cardiac death is the unexpected, nontraumatic, abrupt cessation of effective cardiac function in a patient with either no symptoms or acute symptoms for less than 1 hour.4,5 Prodromal symptoms such as chest pain, palpitations, and fatigue may be present within the preceding 24 hours.4 One half to two thirds of deaths secondary to coronary artery disease (CAD) occur suddenly, usually within 2 hours of the onset of symptoms.1,68 Most victims of sudden cardiac death die before reaching a hospital.1 Although the vast majority of sudden deaths in this country are secondary to CAD, other etiologies may be responsible.

Cardiopulmonary resuscitation (CPR) is utilized to sustain cardiovascular and respiratory function. Related clinical investigations have been analyzed to formulate advanced cardiac life support (ACLS) guidelines for the treatment of sudden death. Until recently, ACLS guidelines have reflected somewhat dogmatic approaches for what has become "standard of care." More recent recommendations were based on available scientific data9 and established by the American Heart Association (AHA) in collaboration with the International Liaison Committee on Resuscitation (ILCOR). ACLS guidelines are now considered recommendations formulated from available scientific data, not mandates for a "standard of care."

It has been estimated that CPR is performed on 1% to 2% of all patients admitted to teaching hospitals (including approximately 30% of patients who die in teaching hospitals).10,11 CPR's underlying goal is to restore spontaneous circulation. Early defibrillation is currently the single most effective means for restoring spontaneous cardiac function and improving survival. When initial attempts fail, restoration of spontaneous circulation (ROSC) is dependent on improving myocardial perfusion combined with treatment of underlying disorders. Novel methods of CPR, circulatory support devices, and new antiarrhythmics may aid in these critical challenges. To date, the survival rates remain disappointingly low,1214 and many patients who are successfully resuscitated suffer severe neurologic impairment.1517


?? TECHNIQUES IN CARDIOPULMONARY RESUSCITATION
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Basic life support (BLS) encompasses the techniques utilized to sustain ventilation and blood flow. BLS measures are recommended until advanced cardiac life support (ACLS) measures are available to restore spontaneous circulation. An ABCD algorithm (airway, breathing, circulation, defibrillation) describes the standardized approach to patients in cardiac arrest (Fig. 16-1).18



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FIGURE 16-1 Universal treatment algorithm for adult emergency cardiac care.

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Airway Management

Unresponsive patients mandate activation of the emergency medical system (EMS). Initial steps are then directed toward ensuring a patent airway.19 The airway can usually be opened using the head-tiltchin-lift maneuver. The jaw-thrust technique is an alternative for suspected neck trauma; however, it is more difficult to perform.20 Both relieve posterior displacement of the tongue, which is the most common cause of airway obstruction.2022 If no signs of respiration are present, rescue breathing is initiated. Difficult ventilation should be addressed by repositioning and addressing airway foreign bodies. The Heimlich maneuver, or subdiaphragmatic abdominal thrust, is recommended for relief of airway obstruction secondary to foreign bodies.23 Rapid thrusts to the subxiphoid region produce high airway pressures, which may dislodge a foreign body.24 This should be repeated until ventilation is established. Alternatively, chest thrusts are recommended for obese patients and women in late stages of pregnancy. Magill forceps can be used to retrieve foreign bodies when these techniques fail. Back blows are recommended only for pediatric patients.24

Masks and oral and nasal airways may be used for mouth-to-mask ventilation or with bag-valve devices. Mouth-to-mask breathing is more reliable in providing adequate tidal volumes than bag-valve-to-mask respiration. 2527 Bag-valve devices reduce exposure to potential infection, but require two or more rescuers.9 Oropharyngeal or nasopharyngeal airways should be used in nonintubated patients. Oropharyngeal airways are not used in conscious patients because of the risk of laryngospasm and regurgitation.9

Endotracheal intubation (ETT) is the preferred method of airway management. In addition to maintaining an open airway, the risk of gastric distension and aspiration is decreased, and an alternative route for drug administration is provided.28 Orotracheal intubation is optimal for resuscitation unless a neck injury is suspected, in which case nasotracheal intubation is recommended. End-tidal CO2 monitors may be used as an adjunct to confirm tube placement. Esophageal intubation is likely in the absence of elevated end-tidal CO2.29,30 Complications of ETT include esophageal intubation, oral trauma, pharyngeal laceration, vocal cord injury, pharyngeal-esophageal perforation, main-stem bronchus intubation, and aspiration.3133

Transtracheal catheter ventilation (TTC) is a temporizing method when other modes of ventilation are not possible. A catheter passed through the cricothyroid membrane is attached to a pressurized oxygen tank (30 to 60 lb/in2), and inspiratory flow is regulated by a triggered valve. TTC provides limited ventilation and can lead to a respiratory acidosis.34 Other problems may include pneumothorax, hemorrhage, and esophageal perforation.35 Cricothyroidotomy is another consideration when endotracheal intubation is not possible.36 Complications of cricothyroidotomy may include hemorrhage, esophageal perforation, and mediastinal and subcutaneous emphysema.37 Tracheostomy is rarely indicated for managing cardiac arrest but should be considered when ventilation cannot be otherwise achieved.

Mouth-to-mouth ventilation is recommended in the absence of airway devices. It is effective38 and generally results in an alveolar Po2 of approximately 80 mm Hg. Chest movement is observed to assess the adequacy of ventilation at a recommended respiratory rate of 10 to 12 per minute.9 Cricoid pressure (Sellick maneuver), maintaining a patent airway, and administering slow breaths may decrease the risk of gastric distension, regurgitation, and aspiration.27,37,39,40 Mouth-to-nose breathing is performed when the mouth cannot be opened or a tight seal is not possible.

There has been great concern about contracting transmissible diseases from cardiac arrest victims during mouth-to-mouth resuscitation, and this fear has reduced enthusiasm for CPR. Barrier devices, such as face shields and mask devices, have been developed to protect EMS personnel from such exposure. Studies indicate minimal risk of the transmission hepatitis B virus (HBV), hepatitis C virus (HCV), or the human immunodeficiency virus (HIV) from CPR procedures.41,42 However, there is a risk of transmission if blood is inadvertently exchanged with an infected victim.43 Therefore, rescuers should always observe universal precautions.41 Herpes44 and tuberculosis19,45 have been transmitted to emergency personnel on rare occasions. When mouth to mouth ventilation is not performed, chest compressions alone are better than no resuscitation attempt. A recent randomized trial found patients who received chest compressions alone experienced no significant difference in survival to hospital admission or discharge compared to CPR including mouth-to-mouth ventilation.46

Closed Chest Cardiac Massage

Closed chest cardiac massage (CCM) remains the principal means of maintaining the circulation during cardiac arrest. CCM is performed with the victim supine on a flat, firm surface (Fig. 16-2). Compressions over the lower half of the sternum are recommended at a rate of 100/min. Compression depth should be 4 to 6 cm and occupy 50% of the cycle.47 Complete release after each downstroke allows ventricular filling, and maintaining hand contact with the chest avoids repositioning between compressions.9 CCM can generate up to 25% to 30% of normal cardiac output.4851 Systolic blood pressures usually range from 60 to 80 mm Hg, while diastolic pressures are typically less than 20 mm Hg.52 Organ perfusion is poor. Cerebral blood flow is reduced to 10% to 15%52 and coronary perfusion 1 to 5% of normal.5355 Clearly, CCM is only a tempory means for providing some blood flow to vital organs. In the absence of definitive interventions (e.g., defibrillation), CCM is unable to sustain life. As the delay to such therapy increases, survival becomes significantly less likely. The possibility of successful ROSC and survival is exceedingly low when CCM is required for more than 30 minutes. However, CCM is the only widely available means of sustaining the circulation while awaiting definitive therapy.



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FIGURE 16-2 Cross-sectional view of closed cardiac massage. Compressions are delivered with high velocity and moderate force, resulting in cardiac compression.

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Discontinuation of CPR

Unfortunately, there are no good criteria for discontinuing CPR efforts. Even determining the adequacy of CCM is quite subjective. Palpable pulses only signify the difference between systolic and diastolic pressures,56 not forward flow. Venous pulse pressures may, in fact, be similar.57 The presence of reactive pupils and/or spontaneous respirations does indicate some cerebral perfusion, but these findings are frequently absent and poorly correlate with outcome.58 Aortic diastolic pressure is a measure of CPR effectiveness.59 Diastolic pressures correlate best with coronary perfusion during CPR.18 Unfortunately, this measurement is usually not available in the clinical setting.

End-tidal CO2 (ETCO2) is a noninvasive alternative for assessing CPR. ETCO2 correlates with flows generated during CPR and provides information regarding proper endotracheal tube placement30,60,61 A low ETCO2 indicates either low blood flow (inadequate CCM), esophageal intubation, airway obstruction, massive pulmonary embolus, or hypothermia.62 Studies have shown that ETCO2 may be predictive of survival in patients suffering from sudden cardiac arrest.63,64

Complications of CPR

Common complications of CCM are rib and sternal fractures.65 Others include aspiration, gastric dilatation, anterior mediastinal hemorrhage, epicardial hematoma, hemopericardium, myocardial contusion, pneumothorax, coronary air embolus, hemothorax, lung contusion, and oral and dental injuries.6567 The liver and spleen are the most commonly injured intraabdominal organs, reportedly in 1% to 2% of cases.65 Rarely, significant injury can involve the trachea, esophagus, stomach, cervical spine, vena cava, retroperitoneum, and myocardium.65


?? SUDDEN DEATH TREATMENT CONSIDERATIONS
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Sudden death generally presents as one of three different pathophysiologic conditions: ventricular fibrillation/tachycardia (VF/VT), asystole, or electromechanical dissociation (EMD), also called pulseless electrical activity (PEA). VF may persist after initial defibrillation attempts ("shock-resistant" or may persist despite multiple therapeutic interventions ("persistent" or "refractory"). Furthermore, VF may be successfully treated by initial ACLS measures and subsequently recur ("recurrent"). These patterns of dysrhythmias 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 (Fig. 16-1).

Ventricular Tachycardia

Ventricular tachycardia (VT) is a reentrant arrhythmia characterized by premature ventricular depolarizations at a rate greater than 100 beats per minute. Cardiac arrest can occur with rapid, sustained VT. Ventricular fibrillation (VF) is characterized by uncoordinated, continuous contraction of the ventricles. Holter monitors have shown that 80% to 90% of nontraumatic cardiac arrests originate with VF/VT.68 Over 90% of survivors in most series have VF/VT as the initial rhythm.69,70 Rapid defibrillation is the most important determinant of survival after cardiac arrest.7174 Therefore, defibrillation should precede all other CPR therapy if a device is immediately available.9 Even minimal delays impact negatively on the success of defibrillation.75,76 Mortality from sudden death increases 4% to 10% for every minute preceeding initial defibrillation attempts.73,75,77 Countershocks delivered more than 10 to 12 minutes after the onset of the arrest result in survival rates that approach zero.78 The current ECC guidelines strongly emphasize early defibrillation and wider use of automated external defibrillation systems.9

Treatment of VF and/or pulseless VT, therefore, begins with immediate defibrillation or CPR until one arrives. Recommended energy for the initial defibrillation is 200 J. The electrodes should remain in place on the chest between defibrillation attempts. If monitored VF continues, a second shock of 200 to 300 J is given immediately. A third countershock of 360 J is likewise delivered if the second is without success. It is vital that the three shocks be given consecutively and without delay for ventilations, chest compressions, or other interventions. CPR is performed whenever the three initial defibrillation attempts fail. The patient is intubated and intravenous (IV) access obtained. Figure 16-3 outlines the subsequent treatment algorithm for persistent VF/VT. Epinephrine or vasopressin is given IV or via the endotracheal tube. Vasopressin has recently been added to the ECC guidelines but should only be given once with no subsequent doses. Defibrillation is attempted again with 360 J. The provider may choose to use three stacked shocks at this point. Epinephrine is given every 3 to 5 minutes throughout the resuscitation. Refractory VF is treated with antiarrhythmic agents (Fig. 16-3). There is growing evidence that amiodarone may be the most efficacious drug in this setting.12,7981 Lidocaine is still acceptable therapy for recurrent VF and pulseless VT; however, there are insufficient clinical data to recommend it over amiodarone.82 Magnesium sulfate, particularly if hypomagnesemia is suspected, and procainamide are recommended for intermittent and/or recurrent VF/VT. Bretylium is no longer recommended. The patient should be given a 360-J shock within 30 to 60 seconds of each drug.9



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FIGURE 16-3 Treatment algorithm for persistent ventricular fibrillation and pulseless ventricular tachycardia (VF/VT).

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The prognosis of patients found in VF/pulseless VT is better than that for asystole or pulseless electrical activity (PEA). Up to 30% of patients who suffer witnessed VF/VT arrests are successfully resuscitated.83,84 Early defibrillation has been shown conclusively to improve survival in out-of-hospital arrest.71,72 Eisenberg et al71 reported survival increased from 7% to 26% when defibrillation was provided in the field. Stults et al72 reported similar findings. Failure of initial defibrillation attempts is a poor prognostic sign. Attention should be focused on correcting underlying disorders including metabolic derangements. Emphasis should also be directed toward ensuring effective CPR, antiarrhythmic therapy, and further attempts to defibrillate before discontinuing resuscitative efforts.9

Asystole

Asystole is complete absence of electrical and mechanical cardiac activity, which frequently indicates a terminal event. However, CPR efforts can result in survival. Attention must be given to a continued search for treatable causes. Other priorities (Fig. 16-4) include establishing effective CPR and rhythm confirmation.85 Fine, low-amplitude VF may masquerade as asystole in certain electrocardiographic (ECG) leads.86 This scenario is thought to be rare, occurring in merely 2.5% of patients diagnosed with asystole in one report.87 More likely, erroneous diagnoses result from incorrect lead placement and equipment malfunction.87 Verifying lead placement and connections while confirming asystole in other leads is important. There is no benefit to countershocks in true asystole88,89; they can only induce a parasympathetic discharge and diminish subsequent chances of restoring circulation.90,91 If fine VF is strongly suspected, defibrillation should be considered.



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FIGURE 16-4 Algorithm for asystole.

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Once confirmed, asystole is approached with basic ABCD guidelines (Fig. 16-4). Epinephrine is the only recommended vassopressor and is administered to raise perfusion pressures.9,92 Vasopressin is not recommended for asystole. Epinephrine is repeated every 3 to 5 minutes during the resuscitation. Atropine is administered every 3 to 5 minutes for a total dose of 0.03 to 0.04 mg/kg. Atropine can treat the high parasympathetic tone that underlies severe bradyasystolic arrests.90,91,93 Transcutaneous or transvenous pacing therapy may also be effective if applied early.94 Pacing should be applied immediately whenever it is considered, otherwise depleted high-energy phosphates will negate effective cardiac contraction despite successful electrical capture.95 Unfortunately, the prognosis of asystole remains grim. Less than 2% of these patients survive to discharge.96 Asystole following countershocks for VF has a better prognosis than asystole occurring after prolonged CPR.97

Pulseless Electrical Activity

Pulseless electrical activity (PEA) also carries a poor prognosis and is characterized by organized electrical activity without effective cardiac contractions. PEA is synonymous with electromechanical dissociation (EMD) and includes conditions such as pulseless idioventricular, bradycardiac, and ventricular escape rhythms.9 These later three dysrhythms have an extremely poor prognosis.98,99 Overall, PEA is the most common proximate cause of death in delayed or difficult resuscitations.85 As recommended for asystole, PEA mandates a careful assessment for reversible causes (Fig. 16-5). Rapid, narrow-complex activity increases the probability for treatable conditions.85,100 Successful resuscitation is otherwise very unlikely. Effective CPR and epinephrine to augment perfusion pressures remain important.99,101103 Atropine is indicated for bradycardia.9 Patients with chest trauma should undergo emergency left anterolateral thoracotomy104 to address potentially reversible disorders, including cardiac tamponade and cardiovascular injuries. Thoractomy also provides exposure for direct cardiac massage and occlusion of the descending thoracic aorta, which may be lifesaving in the trauma setting.



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FIGURE 16-5 Treatment algorithm for pulseless electrical activity (PEA)

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Cardioversion

Electrical cardioversion is the only effective treatment for ventricular fibrillation (VF). Defibrillation depolarizes the entire heart, resulting in temporary asystole.91,105 Pacemaker cells are then able to restore rhythmic myocardial activation. Myocardial contraction can resume if high-energy phosphate (HEP) stores, depleted rapidly during CPR,106 are sufficient.107,108 Although CPR can provide some organ perfusion, early defibrillation remains paramount. The probability of successful defibrillation approaches 90% immediately following a witnessed arrest.106,109,110 Success rates then decline rapidly. The likelihood of restoring spontaneous circulation decreases 7% to 10% every minute.78 At best, current CPR can only slow the already deteriorating state. Once a defibrillator is available, it should be attached immediately. When positioned on the chest, quick-look paddles allow rhythm evaluation and VF or pulseless VT treated immediately. Blind defibrillation is rarely indicated due to the wide availability of quick-look paddles. Countershocks for VF or pulseless ventricular tachycardia are delivered asynchronously. Shocks should be synchronized for relatively stable rhythms such as atrial fibrillation/flutter and monomorphic VT.9 Otherwise, asynchronous countershocks may impinge on the relative refractory period, which risks inducing VF.111

Energy levels used for cardioversion are important for successful defibrillation. Low currents may be ineffective, while excessive energy levels can result in myocardial injury.112,113 Generally, the lowest energy level for reliable defibrillation is preferred. A prospective study demonstrated that 175 J and 320 J were equally effective during the first defibrillation attempt.114 Based on these data, 200 J is recommended for initial defibrillation attempts.9 Up to 90% of adults can be successfully defibrillated when 200 J is delivered sufficiently early.115,116 The range for a second countershock is 200 to 300 J. Decreased transthoracic impedance following repetitive shocks explains the consideration for 200 J during second attempts,117,118 as subsequent countershocks would be expected to deliver greater energy to the heart. However, increasing energy levels to 300 J may provide more reliable increases in current delivery.117

Body size, which is not considered in current guidelines, also impacts on defibrillation energy requirements.9 The optimal current for defibrillation is 30 to 40 A.119121 Adults have an average transthoracic impedance of 70 to 80 gV, requiring a 200-J countershock to produce a 30-A current.122 However, the range of impedance varies significantly117121 and depends on many factors, including the energy, chest size, electrode size, interelectrode distance, paddle-skin coupling, phase of respiration, and antecedent countershocks.117,118,123,124 Therefore, the defibrillation technique is important. Electrodes are positioned to maximize current flow using three paddle arrangements. Most commonly, one electrode is placed on the right parasternal border below the clavicle and the other is positioned in the left midaxillary line, level with the nipple. Alternatives are anteroposterior and apical-posterior positioning.9 Electrodes must not touch directly or via conductive gels to ensure that current passes through the heart. During open chest resuscitation, one internal paddle is placed over the right ventricle, and the other is placed behind the apex. Larger paddles result in lower resistance.117,124 Most adult paddles are 8 to 12 cm in diameter. Smaller paddles have high impedance and should be used only if standard adult paddles do not fit in the chest.125

Defibrillation threshold (DFT) describes the amount of current required to defibrillate the heart. DFT increases with CPR time. The most important factor affecting the DFT is coronary perfusion pressure. Catecholamines decrease the DFT.126128 It was once thought that epinephrine decreased the DFT through its beta-adrenergic effects. However, epinephrine's beneficial effect on DFT is due primarily to increased coronary perfusion pressure (alpha-adrenergic receptor stimulation).129 The underlying mechanism of the time-dependent increase in DFT during VF is not completely understood. The DFT is not affected by metabolic or respiratory acidosis.130,131 Recent work implicates adenosine, via adenosine A1 receptor antiadrenergic effects, as a possible mediator of the increase in DFT with time.132 Cardiac compression has been shown to reduce defibrillation thresholds during open chest defibrillation.133 Aminophylline, an adenosine receptor antagonist, decreases the defibrillation threshold.134136

Patients with pacemakers and automatic internal cardiodefibrillators (AICDs) deserve careful consideration. Patients with pacemakers should not have the paddles placed directly over the generator,137 and must be interrogated to determine pacing thresholds after defibrillation. Patients with AICDs who present with VF or pulseless VT should have external defibrillation performed immediately.138 AICDs are shielded to withstand external countershocks. AICD patches may increase transthoracic resistance.139 Therefore, the electrode position should be changed if initial countershocks fail. After successful external defibrillation, the AICD unit should be tested.

New automated external defibrillators (AEDs) are being increasingly utilized. The AED analyzes the ECG pattern, and then sounds an alarm and discharges when VF is detected. AEDs require less training than conventional defibrillators, and there is less delay in administering the countershock.78,140,141 Several studies with AEDs have shown equivalent or improved survival compared with early defibrillation using manual defibrillators.142144 AEDs are endorsed by the AHA for use in out-of-hospital arrest.145

Current-based defibrillators have been developed in an effort to improve defibrillation.119,120,146 These devices should significantly enhance the delivery of appropriate energy to the myocardium and increase the likelihood of successful cardioversion while reducing the risk of myocardial trauma. Other areas of investigation include delivery of biphasic (bidirectional) or multipulse, multipathway shocks.122 These methods are in use for internal defibrillators, but their efficacy for external defibrillation has not been established.147,148

A precordial thump is an alternative means of attempting defibrillation and may be used for witnessed arrests when a defibrillator is not immediately available. It has been reported to convert VT to sinus rhythm in 11% to 25% of cases.149,150 Unfortunately, precordial thumps may convert VT to VF, asystole, or EMD,150,151 and are very unlikely to convert VF. A precordial thump is not indicated for unwitnessed or out-of-hospital arrests.9


?? PHYSIOLOGY OF CARDIOPULMONARY RESUSCITATION
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The mechanism(s) generating forward blood flow during CPR has been a subject of significant controversy. Kouwenhoven postulated that chest compressions are translated directly to the heart through the sternum and spine.152,153 This mechanism became known as the cardiac pump. Multiple laboratory and clinical investigations have verified this as an operative mechanism during closed chest compression.154157 However, other operative mechanisms have also been demonstrated during CPR.

Investigations have identified at least two other important mechanisms responsible for blood flow during CPR. The thoracic pump was discovered by the observation that coughing during cardiac arrest generated forward flow. Laboratory51 work has demonstrated chest compressions cause a general rise in intrathoracic pressures capable of forcing blood into the systemic circulation. The heart in this circumstance merely functions as a conduit. Many studies have validated the thoracic pump mechanism during CPR.48,158160

A third means for generating blood flow during CPR is the abdominal pump. This describes the effects of abdominal compressions, which are now advocated for CPR.161164 The abdominal pump operates through arterial and venous components. The arterial component reflects compression of the abdominal aorta, which forces blood into the peripheral circulation. The aortic valve remains closed during abdominal compression and resists retrograde arterial flow. Simultaneously, the venous component pushes blood from the inferior vena cava into the right heart. Both contribute added hemodynamic benefits during recommended techniques for abdominal compressions in CPR.

It is clear that the cardiac, thoracic, and abdominal pump mechanisms are all important means for generating forward flow during CPR. Technique dictates to what extent these three mechanisms contribute. Other factors that can influence the effectiveness of these pumping 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. The pump mechanism that contributes most toward effective CPR is widely variable. Better understanding of these variables should guide recommendations and improvements in CPR techniques and adjunctive devices.


?? CPR TECHNIQUES AND MECHANICAL ADJUNCTS
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The high mortality rates associated with cardiac arrest have led to increased enthusiasm for several techniques and devices. Combining chest and abdominal pumping techniques within the same compression cycle is termed interposed abdominal compression CPR (IAC-CPR). The technique employs chest compressions with abdominal compression during the relaxation phase of chest compression (Fig. 16-6). The simplest and most studied applications involve compressing the chest and abdomen at equal durations. The method has not been associated with increased intra-abdominal injuries or aspiration. Human studies of IAC-CPR have yielded encouraging results with statistically significant improvement in outcome measures.165177 Return of spontaneous circulation and survival to discharge were both improved using IAC-CPR when examining inpatient cardiac arrests.166,168,169 Therefore, the method is now considered an acceptable alternative to standard CPR for in-hospital arrests. A device that will allow IAC-CPR by a single rescuer is currently under evaluation (Fig. 16-7).



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FIGURE 16-6 Interposed abdominal compression (IAC) cardiopulmonary resuscitation (CPR), or IAC-CPR.

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FIGURE 16-7 Device proposed for abdominal compression cardiopulmonary resuscitation (IAC-CPR).

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Noninvasive Mechanical Devices

Noninvasive mechanical devices have recently been developed for improving CPR. A pneumatic vest optimizes the thoracic pump mechanism by alternating pressures around the thoracic cage (Vest-CPR). Vest-CPR utilizes a pneumatic bladder tailored to fit the chest. Air is forced into and out of the vest by a pneumatic drive. Two clinical trials demonstrated improved outcomes with an increased rate of return of spontaneous circulation.170,171 However, no patients survived to discharge and complete results have not yet been published. The vest is considered an acceptable alternative to standard CPR for ambulance transport or for in-hospital use.

Active Compression-Decompression

Active compression-decompression (ACD) is a promising means for improving CPR. The concept originated from successful resuscitations using a plunger.172 A device that consists of a hand-held suction cup with a central piston and handle is required (Fig. 16-8). ACD-CPR can increase aortic pressures resulting in improved cerebral, coronary, and renal blood flow.173176 Ventricular filling and venous return are augmented by negative intrathoracic pressure during the active decompression phase.177 Two initial studies reported increased return of spontaneous circulation and 24-hour survival with the ACD device. Survival to discharge was higher with ACD in both studies but did not reach statistical significance.178,179 Data from 2866 patients using the ACD device were subsequently combined.180 ACD improved 1-hour survival but long-term outcome was not significantly different from standard CPR. More recently, a randomized clinical trial demonstrated significantly improved 1-year survival following ACD compared to standard CPR.181 ACD-CPR is considered an acceptable alternative to standard CPR.



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FIGURE 16-8 Active compression-decompression cardiopulmonary bypass (ACD-CPR) using a suction cup device attached to chest wall.

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Open Chest Cardiac Massage

Several invasive means of supporting the circulation are also advocated for resuscitation. Open chest cardiac massage (OCM) was relatively common prior to 1960.182 The role for OCM is currently limited to specific circumstances. OCM is indicated for cardiac arrest associated with penetrating thoracic trauma. Other situations in which OCM should be considered include cardiac arrest due to hypothermia, massive pulmonary embolism, pericardial tamponade, or intra-abdominal hemorrhage, and when chest deformity precludes effective CPR. The recommended approach is via a left lateral thoracotomy except following recent cardiac surgery where the prior sternotomy can be reentered. Thoracotomy is carried through the fifth intercostal space and the pericardium opened anterior and parallel to the phrenic nerve. The heart is compressed with two hands or, alternatively, with one hand while the other is used to occlude the thoracic aorta (Fig. 16-9).



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FIGURE 16-9 Technique of open chest cardiac massage. The heart is exposed via an anterolateral thoracotomy through the fifth intercostal space. The pericardium is opened if there is evidence of pericardial tamponade; otherwise, it is left intact. The heart is massaged at a rate of 60 to 80 beats per minute.

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Numerous studies have demonstrated superior hemodynamics results during open massage compared to CCM.56,183188 Most notable are increased diastolic pressures and reduced central venous pressures,56,185,188 which demonstrated the favorable effects on coronary perfusion during OCM versus CCM. Cardiac output and cerebral blood flow are also higher during OCM,186,187,189 and OCM has resulted in successful resuscitation following failed attempts during CCM.189191 However, clinical results are not improved when OCM is used following prolonged CPR efforts.192 Animal studies have suggested that OCM may improve results if applied early after a short period of ineffective CCM.193 And a recent prospective, nonrandomized clinical trial emphasized the importance of instituting OCM earlier to improve outcome.194 Patients receiving OCM had improved outcome compared to CCM; however, improvements declined as the period of CCM increased.

Early application of OCM may improve survival. For results to be meaningful, this needs to be determined in a prospective clinical trial. Downtimes prior to thoracotomy must also be minimized to reduce neurologic impairment in survivors. Potential complications of OCM include right ventricular perforation, hemorrhage, lung laceration, phrenic nerve injury, esophageal and aortic injury, cardiac lacerations, and empyema.191 However, the rate of infection is relatively low, approximately 5%, given the emergent nature of the procedure on an unprepped chest.195

Blood Pumps

Blood pumps can also improve resuscitation results. Hemodynamics, survival, and neurologic function are improved in animals treated with early CPB versus those treated with standard CCM.196198 However, these devices are generally limited to tertiary care centers. A number of institutions have utilized CPB to selectively bridge patients to transplantation following cardiac arrest.199201 The development of portable CPB systems has made the technology more available and CPB has been used successfully in a growing number of centers for select cases of cardiac arrest.202208 Growing clinical experience has demonstrated improvements in outcome when CPB is applied within 20 to 30 minutes following cardiac arrest, with long-term survival ranging from 17% to 57%. A registry has reported a 27% survival rate when CPB systems were used for the treatment of 386 patients in cardiac arrest.209 The possibility of survival appears limited to patients who receive CPB within 30 minutes of a witnessed normothermic arrest. Hypothermic cardiac arrests represent a unique category in which survival is possible following relatively prolonged arrests. In this setting, CPB has been advocated as the resuscitation method of choice because of its unique ability to rewarm the patient while providing total circulatory support.165,166 Although treatment protocols have not been well defined, CPB support should be continued until the patient is adequately rewarmed before resuscitative efforts are abandoned.

The intra-aortic balloon pump IABP can improve hemodynamic parameters during CPR.210,211 However, the value of IABP augmentation during CPR appears very limited. Alternatively, there has been growing interest in using aortic balloon occlusion catheters.212214 Selective aortic arch perfusion utilizes a catheter inserted via the femoral artery and advanced to the descending thoracic aorta. Balloon occlusion allows selective, retrograde perfusion of the heart and brain. One proposed advantage is that therapeutic agents could be selectively delivered to the heart and brain by this technique.

Direct Mechanical Ventricular Actuation

Direct mechanical ventricular actuation (DMVA) is a unique nonblood contacting method of circulatory support that transfers systolic and diastolic forces directly to the ventricular myocardium (Fig. 16-10). DMVA employs a pneumatically regulated heart cup constructed with a flexible inner membrane and semirigid shell. The device is vacuum attached to the heart via a left anterior thoracotomy. Ventricular compression results in physiologic forward blood flow while active decompression enhances diastolic filling.215 DMVA can provide hemodynamic support far superior to any other CPR method. Its capability to provide physiologic pulsatile flow may best explain improved neurologic outcome when compared with CPB in animal models.216218 DMVA is uniquely capable for resuscitation because it can be applied rapidly. One disadvantage is the requirement for a thoracotomy; however, DMVA's value as an adjunct in resuscitation is complemented by its versatility and lack of blood contact. Clinical experience with DMVA has resulted in successful bridge to transplantation, postcardiotomy support, and long-term recovery from severe myocarditis.219,220



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FIGURE 16-10 Direct mechanical ventricular actuation (DMVA). The ventricles are encompassed by a pneumatically regulated heart cup and the arrested heart is compressed (right) and dilated (left).

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?? PHARMACOLOGIC THERAPY DURING CPR
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Peripheral venous access is preferred for purposes of speed and safety and for avoiding CPR interruption. Drugs take 1 to 2 minutes to reach the central circulation during CPR221 and should be administered as boluses followed by a 20-mL saline flush with extremity elevation.222 Peak drug concentrations are lower with peripheral than central venous injection.223 Central access should be considered if the response to peripherally administered drugs is absent. The internal jugular and supraclavicular sites are preferred to the femoral vein because return from the infradiaphragmatic IVC is impaired during CPR.224 A long femoral line that extends above the diaphragm overcomes this problem. Intravenous fluids are not indicated for routine cardiac arrest without hypovolemia. Fluid administration may adversely affect coronary perfusion pressure and myocardial blood flow by raising right atrial pressure.225 Fluids can benefit in certain cases of PEA, such as hypovolemia and cardiac tamponade.

When venous access is not possible, drugs may be administered via an endotracheal tube. The medications are given via a catheter passed beyond the tip of the ETT. The dose is 2 to 2.5 times the recommended intravenous dose, diluted in 10 mL of saline or distilled water.226 Water provides better absorption but has a greater adverse effect on Pao2 than saline.227 Several rapid insufflations are given after the bolus to disperse the drug. Intracardiac injection is not recommended for routine use during CPR. It may be used for epinephrine during OCM or when no other access can be obtained during CCM. Disadvantages of intracardiac injection are the need to stop CPR and the high rate of complications. Complications include coronary artery laceration, cardiac tamponade, and pneumothorax.

The principal pharmacologic agents recommended for ACLS have been adrenergic agonists, antiarrhythmics, and buffers. Until recently, alpha-adrenergic agonists have been the only class of drugs that have been shown to improve outcome definitively in CPR.228230 The primary benefit is vasoconstriction. Increases in peripheral resistance result in elevated aortic pressure, which improves coronary perfusion. Epinephrine is given for this purpose during cardiac arrest.129,229232 Epinephrine's beta-adrenergic effects have not been clearly shown to benefit the treatment of cardiac arrest. The recommended dose of epinephrine for resuscitation is 1.0 mg IV every 3 to 5 minutes throughout the resuscitation attempt.9 Epinephrine has improved the return of spontaneous circulation and survival rate in animal models of cardiac arrest.228230 The minimum coronary perfusion pressure and myocardial blood flow needed to achieve successful defibrillation are 15 mm Hg and 15 to 20 mL/min per 100 g, respectively.52,85 Standard CPR techniques rarely achieve these requirements in the absence of pressor agents. Anecdotal reports of using higher doses of epinephrine generated enthusiasm.233235 Subsequent clinical trials reported higher rates of ROSC, but no significant survival benefit.236240 One trial found high-dose epinephrine had more adverse effects,237 which may be partly explained by increases in oxygen demand.241

A number of other nonadrenergic vasocontrictive agents have been studied in an effort to find a more effective drug then epinephrine. Vasopressin has recently emerged as an alternative to epinephrine for treating cardiac arrest. Comparative laboratory and clinical data indicate that vasopressin may be preferable to epinephrine.242,243 Although further clinical trials are needed, vasopressin is now considered an acceptable alternative to epinephrine for initial treatment of the arrested patient.

The effectiveness of antiarrhythmic agents in the treatment of sudden death has not been well substantiated in previous clinical investigations. Recently, randomized clinical trials have demonstrated amiodarone to be effective in the treatment of cardiac arrest.12,80,81,244 Amiodarone significantly improved survival to hospital admission compared to placebo for VF/pulseless VT.244 It was found to be as effective as bretylium for treating VF or unstable VT in another randomized trial. Most recently, amiodarone significantly increased survival to hospital admission compared to lidocaine in a randomized clinical trial for the treatment of sudden death.12 There was a trend toward increased survival at hospital discharge with amiodarone that did not reach statistical significance. Amiodarone is now recommended for the treatment of persistent VT and/or VF after defibrillation and epinephrine. Currently, lidocaine has more evidence opposing than supporting its use in cardiac arrest.82 However, it is considered an acceptable alternative to amiodarone.

Procainamide is a ganglionic blocker that slows phase-4 depolarization and intraventricular conduction. It is recommended for recurrent VF/VT and should be administered as an infusion over 30 minutes. Rapid infusion rates are associated with hypotension.245 Procainamide may be of little benefit during cardiac arrest and also may worsen ventricular arrhythmias in the presence of hypokalemia and hypomagnesemia.

Magnesium sulfate should be administered for suspected hypomagnesemia or torsades de pointes. It is recommended for treatment of refractory VF/VT. Hypomagnesemia is associated with ventricular arrhythmias and sudden cardiac death246 and may hinder potassium replenishment in hypokalemic patients. Common side effects of magnesium sulfate include flushing, mild bradycardia, and hypotension with rapid infusions. Hypermagnesemia can cause flaccid paralysis and cardiorespiratory arrest.

Atropine is a parasympatholytic agent that enhances atrioventricular node conduction and sinus node automaticity. It is indicated for symptomatic bradycardia and asystolic arrest.90,91,93,247 Asystole secondary to prolonged ischemia is almost uniformly fatal, and although atropine is unlikely to be of real benefit, there is no evidence that it is harmful under these dire circumstances.97 The dose of atropine in cardiac arrest is 1 mg as an IV bolus, repeated every 3 to 5 minutes to a total dose of 3 mg. For symptomatic bradycardia, the dose is 0.5 to 1 mg (maximum of 2 to 3 mg). Doses lower than 0.5 mg are avoided because they may cause paradoxical bradycardia.248,249 Adverse effects of atropine include tachycardia and anticholinergic effects.

Sodium bicarbonate is recommended for acidosis during cardiac arrest. It binds hydrogen ions to form carbonic acid, which is converted to CO2 and eliminated by the lungs. During CPR, CO2 may accumulate rapidly, leading to a hypercarbic venous acidemia.250,251 Since CO2 is diffusible across membranes, paradoxical intracellular acidosis252 may result and decrease the likelihood of successful resuscitation. Additionally, hypocarbic arterial alkalemia251 or the so-called venoarterial paradox may develop. Sodium bicarbonate may increase CO2 levels, worsen the venoarterial paradox, and exacerbate intracellular acidosis.253,254 Other potential adverse effects of NaHCO3 include alkalemia with a leftward shift of the oxyhemoglobin desaturation curve (less O2 release to tissues), hyperosmolality, hypernatremia, and decreased coronary perfusion pressure.255258 Bicarbonate has not been shown to improve results in cardiac arrest256,257,259 and is only recommended for patients with preexisting acidosis, hyperkalemia, or tricyclic antidepressant overdose. Otherwise, bicarbonate should be considered for prolonged resuscitations.


?? CEREBRAL PROTECTION/RESUSCITATION
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The objective of CPR is to restore circulation in a neurologically intact individual. The main priority during CPR is to provide sufficient myocardial and cerebral blood flow to prevent irreversible damage prior to definitive intervention. Unfortunately, this goal often is not achieved. Less than 10% of CPR attempts result in survival without neurologic damage, whether in or out of a hospital.260

Following cardiac arrest, consciousness is lost within 10 seconds.261 High-energy phosphates and glycogen stores are depleted within 5 minutes.262 Lactic acid accumulates in neurons and has a direct cytotoxic effect.263 The limited cerebral blood flow generated by CPR may exacerbate intracellular acidosis by allowing anaerobic metabolism.264,265 Survival with normal neurologic function becomes unlikely as irreversible brain damage can occur within 4 to 5 minutes of cardiac arrest.266,267 Restoring circulation within 5 to 20 minutes of sudden death is associated with variable degrees of neurologic damage.266,268,269

During CPR, venous valves at the thoracic inlet prevent the transmission of high intrathoracic pressures to the jugular venous system.270 Cerebral blood flow is usually kept at about 50 mL/min per 100 g by autoregulation when cerebral perfusion pressures are within the normal physiologic range.260 CPR results in much lower cerebral perfusion pressures, which seldom exceeded 40 mm Hg.18,52 Cerebral blood flow is only 10% to 15% of normal,185 which may be more harmful than no flow at all.265

Irreversible neuronal injury begins after 5 minutes of ischemia.266 Because neurons can function in vitro for up to 60 minutes of ischemia,271 reperfusion may be as important to neurologic outcome as ischemia itself. Reperfusion injury following successful resuscitation has been termed the postresuscitation syndrome and appears to be multifactorial. Calcium overload in the mitochondria, free-radical injury, and the no-reflow phenomenon may all contribute to reperfusion injury.260 The no-reflow phenomenon describes continued hypoperfusion that may last up to 3 hours.272 Platelet aggregation, altered calcium flux, vasoconstriction, and pericapillary edema are all presumed causative factors.273 Intracranial pressure may not be an important factor as it usually returns to normal soon after cardiac arrest.274,275 Cerebral blood flow remains depressed for 18 to 24 hours following a severe ischemic insult.276 Subsequent periods of hypoperfusion are believed secondary to calcium-induced precapillary vasoconstriction.277

Cerebral blood flow is abnormal following ischemic injury.278 Perfusion is more dependent on arterial pressure and moderate hypotension may lead to further cerebral injury. 279 Patients should be kept normotensive and/or mildly hypertensive in the postresuscitation period.280,281 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 should be given as needed for seizures, which can be subtle and occur in up to 30% of patients.282,283 Body temperature is kept low to normal to reduce cerebral metabolic demand.283

Mild hypothermia has exhibited increasing promise in the prevention of brain damage following cardiac arrest. Earlier experiments using canine models demonstrated improved neurologic function when active cooling followed arrest.284,285 Clinical trials have subsequently shown cooling shortly following resuscitation from cardiac arrests improves neurologic outcome.286 Benefits of hypothermia may be greatest when rapid postresuscitation cooling is achieved and maintained for an extended period.287,288

Although not well proven, there are other considerations for treating patients in the immediate postresuscitation period. The patient should be monitored closely. Supplemental oxygen and intravenous fluids are given, and urine output is monitored. Patients revived using antiarrhythmic agents should have these agents continued as an infusion. Tachyarrhythmias are the most commonly encountered postresuscitation arrhythmias and are likely secondary to increased circulating catecholamines. Increasing emphasis has been placed on the use of beta-adrenergic blockade in the postresuscitation period.289 These agents should be considered unless bradycardia is a significant problem. Bradycardia following CPR frequently requires the airway and ventilatory status to be carefully assessed, followed by adminstration of atropine, epinephrine, and/or pacing if the patient becomes hypotensive.

Possibly the greatest impact on survival has been the use of automatic internal cardiodefibrillators and antiarrhythmics in patients who are at increased risk for sudden death. Multiple clinical studies have now shown that survival can be significantly improved with these devices.146,290294 Amiodarone has also been shown to be effective in this regard.295300 More attention is being directed toward identifying patients who should be considered for such therapy.295,301306 To date, many of these treatments have been directed towards patients who have been successfully resuscitated from sudden death.

Predicting which patients are likely to survive during resuscitation efforts remains an elusive problem. Patients presenting in VF/VT have a better prognosis compared with those in asystole or PEA.10,307311 Advanced age was a negative prognostic indicator in several early series312,313 but has no independent predictive value when comorbidities are considered.10,11 Location of the arrest (ICU versus non-ICU) may be an important consideration.10,11,310,313,314 Patients with noncardiac disorders are more likely to survive if their clinical status was stable prior to cardiac arrest compared to those who were deteriorating.315 Comorbid conditions associated with more than 95% of mortalities after cardiac arrest include renal failure, metastatic cancer, pneumonia, sepsis, hypotension, stroke, and homebound lifestyle.10,307310 Survival is clearly more likely for witnessed arrests and for CPR initiated within 5 minutes, with CPR durations of 15 minutes or less. Mortality increases from 44% for resuscitations less than 15 minutes in duration versus 95% for those that are longer.10 Survival is rare after 30 minutes of CPR.10,316,317

In contrast to inpatient arrest, in which comorbid diseases play a major role in outcome, delayed therapy outweighs all other factors for out-of-hospital arrest. Key determinants of survival include the initial rhythm, witnessed arrest, downtime prior to CPR, and delays in definitive treatment. Survival rates are highly variable among reported series. Becker et al318 found a 2% overall survival to discharge in metropolitan Chicago. In New York City, Lombardi et al319 found a 1.4% survival rate, which improved to 5.3% in patients with witnessed VF arrest. Eisenberg et al320 reported a 22% survival in patients with witnessed arrests; however, downtimes were much shorter. The last study emphasized the importance of early intervention as only 4% of patients suffering unwitnessed arrests survived. CPR initiated within 4 minutes improved survival rates from 12% to 28%. Early definitive care was also associated with improved outcome.320 As with in-hospital arrest, presenting rhythm was a major determinant for survival, with VF/VT having the best prognosis.321 Bystander CPR has repeatedly been associated with improved survival rates for victims of cardiac arrest.322330 In addition, several studies found less neurologic morbidity in cardiac arrest victims who received bystander CPR.327,328,331,332 The decrease in hospital mortality from bystander CPR is primarily due to fewer deaths from anoxic encephalopathy during postresuscitation hospitalization.328,332 Return of consciousness within 24 to 48 hours of arrest is a positive neurologic prognostic sign.10,333,334

Long-term survival of those patients discharged after out-of-hospital arrest is reasonably good. The reported 1-year survival rate ranges from 75% to 85%, and approximately 50% are still alive at 4 years335 (Table 16-1). The majority of these patients ultimately die of cardiac causes.16,336,337 Positive predictors for long-term survival are cardiac arrest associated with acute MI, no prior history of MI, and short time intervals between arrest, CPR, and definitive care.338340 Patients with primary antiarrhythmic events, congestive heart failure, impaired LV function, extensive CAD, and complex premature ventricular depolarizations are less likely to survive long term after discharge.341


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TABLE 16-1 Long-term survival following CPR

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Unfortunately, only a small proportion of patients who suffer sudden death survive and have a subsequent good quality of life.335 Depression is a common problem following discharge but usually resolves within a few months.10 The rate of significant mental impairment in those who survive is variable. Significant neurologic impairment usually results in death prior to hospital discharge. Of those who survived to discharge, a significant proportion have neurologic deficits (Table 16-2).342 For patients who did not receive early intervention, the outlook is more dismal.16,343


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TABLE 16-2 Studies reporting morbidity of patients from out-of-hospital cardiac arrest after resuscitation and discharge

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?? ETHICAL CONSIDERATIONS
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Resuscitation efforts should be discontinued when continued ACLS efforts do not result in a perfusing rhythm.344 Discontinuation is generally based on clinical judgement.345 Unilateral determination of medical futility is made when the patient's underlying medical condition precludes successful resuscitation. Metastatic cancer and sepsis are examples of such conditions.346 Although several studies show that resuscitation for longer than 30 minutes is unlikely to result in long-term survival, there are many anecdotal reports of neurologically intact survival following prolonged resuscitations.10,316,317


?? CONCLUSION
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Until recently, the only factors that have proven to impact CPR favorably are early defibrillation, effective BLS, and epinephrine. Yet overall survival rates remain dismally low. There is a growing pool of evidence that novel methods of CPR and new antiarrhythmics may significantly improve survival in this challenging field. The combination of improved response times, automatic defibrillators, more effective circulatory support methods, and new antiarrhythmic agents has exciting implications. Major improvements in survival and neurologic outcome of out-of-hospital cardiac arrest victims will require continued focus on rapid response and the availability of definitive treatments in the field. Heightened community awareness and organized medical efforts can have a positive impact on these factors.

Future improvements in the field of cardiopulmonary circulation will depend on the timely implementation of promising therapies. Efforts to identify patients at risk for sudden death may provide increasing opportunity for preventative strategies such as AICDs and antiarrhythmics. Most important will be the continued use of well-designed clinical trials to better direct treatment strategies based on valid scientific data.


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