Current concepts in cardiopulmonary resuscitation

Current Concepts in Cardiopulmonary Resuscitation N o r m a n E, Torres, MD, and Roger D, White, MD The "chain of survival" is important in the resuscitation of a patient who has had a cardiac arrest. The provision of Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) is essential in this "chain of survival." Both BLS and ACLS have undergone several revisions since their initial inception. This article reviews (1) the current established and investigational issues of cardiopulmonary resuscitation, (2} the incidence and outcomes of anesthesia-related cardiac

arrest, (3) the use of cardiopulmonary bypass in resuscitation, and (4) cerebral protection during and after resuscitation. Copyright © 1997 by W.B. Saunders Company

HE IMPORTANCE of cardiopulmonary resuscitation (CPR) has been noted throughout ancient literature 1 and history. Alexander the Great was noted for performing a tracheotomy with a sword on a choking soldier. 2 Andreas Vesalius (1555) described "an opening just be attempted in the trunk of the trachea, into which a tube of reed or cane should be put; you will then blow into this, so that the lung may rise a g a i n . . , the lung will swell to the full extent of the thoracic cavity, and the heart becomes strong . . . . -3 Kouwenhoven et al 4 were credited with the initial description of a closed chest cardiac massage technique, which formed the basis of CPR. Current CPR guidelines originated in 1966 from the National Academy of Sciences-National Research Council Conference and have undergone numerous revisions since then based on clinical and research data. 5 The purpose of this article is to review current concepts of CPR based on the American Heart Association (AHA) Basic Life Support (BLS) 6 and Advanced Cardiac Life Support (ACLS) 7 texts and current literature.

and hypercarbic (3.5 to 4.0%7 gas mixture. 12 The independent effects of hypoxia and hypercarbia on the outcome of CPR were investigated by Idris et al. 13 Different gas mixtures were used during CPR on swine: 85% 02 (control group); 10% 02 and 90% N2 (hypoxic group); and 5% CO2 and 95% 02 (hypercarbic group). The control group had a higher resuscitation rate (seven of eight animals) than the hypoxic and hypercarbic groups combined (one of six animals). 13 Hypercarbia has been shown to have a negative inotropic effect on isolated chick myoc.vtes.14 More investigations are necessary to clarify the effect of mouth-to-mouth ventilation on CPR. Unsuccessful CPR has been associated with pulmonary aspiration of gastric contents. 15 The risk of pulmonary aspiration increases with prolonged CPR in the setting of an unprotected airway. To reduce gastric distention during artificial ventilation in a nonintubated patient, high peak inspiratory pressure is avoided by the use of a slow inspiratory phase of 1.5 to 2 seconds. 16Furthermore. during 2-person CPR, a pause after the fifth compression allows for ummpeded ventilation and reduced peak airway pressures. 17 Before endotracheal intubation, mask ventilation with an anesthesia bag, bag-valve-mask, or oxygen-powered positivepressure device may be used. Endotracheal intubation with a cuffed tube is the gold standard for establishing a patent, protected mrway in the critically ill patient. TM Temporizing devices are available for rapid airway control. These alternatives include the esophageal obturator airway, esophageal gastric-tube mrway, pharyngotracheal airway, and esophageal tracheal combitube (Figs 1 and 2). 7'19'20 The laryngeal mask airway (LMA] is useful in providing an airway and ventilating patients under controlled conditions. 21 However, the LMA may not protect the airway from aspiration of gastric contents in an arrested patient. 2z23 One multicenter study observed that of a total of 164 cardiac arrest patients initially managed with an LMA, gastric regurgitation occurred in 20 cases (12%) before LMA insertion, three cases (2%) during use of LMA, and 10 cases (6%) after removal of LMA. 24 Further studies are needed to delineate the use of the LMA during CPR. The American Society of Anesthesiologists (ASA) has outlined an algorithm for the management of the difficult airway. 22 This algorithm lists the cricothyroidotomy with transtracheal jet ventilation as an alternate technique of ventilating the patient

T

BASIC LIFE SUPPORT Cardiopulmonary resuscitation should be initiated whenever an individual cannot adequately oxygenate or per(use vital organs. The goal of effective CPR is to provide oxygenated blood to the systemic circulation and to maintain perfusion to vital organs until spontaneous circulation can be reestablished. Ventilation, circulation, and CPR assessment are reviewed with reference to current literature. AIRWAY MANAGEMENT AND VENTILATION The establishment of an airway and provision of pulmonary ventilation are essential in maintaining oxygen delivery to vital organs during a cardiac or respiratory arrest. The equipment and techniques employed during resuscitation depend on the clinical setting. Initial airway control can be achieved with the head tilt-chin lift. 7,8 The primary cause of airway obstruction in an unconscious or deeply anesthetized human is the epiglottis rather than the tongue. 9 Maneuvers such as the head tilt-chin lift help clear the airway of this obstruction by displacing the hyoid bone anteriorly, which then displaces the epiglottis away from the posterior wall of the pharynx. If this technique is inadequate, the use of an oral or nasal airway may facilitate the establishment of an airway. 1° Mouth-to-mouth or mouth-to-mask techniques may be used in the initial airway management for either in-hospital or out-of-hospital settings, u Recent literature raises the controversy of possible detrimental effects of mouth-to-mouth resuscitation in the early phases of CPR. Mouth-to-mouth resuscitation has been shown to deliver a hypoxic (16.4 to 17.8% oxygen)

KEY WORDS: cardiopulmonary resuscitation, advanced cardiac life support

From the Mayo Clinic and Mayo Medical School, Rochester, MN, Address reprint requests to Roger D. White, MD, Department of Anesthesiology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. Copyright © 1997 by W.B. Saunders Company 1053-0770/97/1103-001753.00/0

Journal of Cardiothoracic and Vascular Anesthesia, Vol 11, No 3 (May), 1997:pp 391-407

391

392

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who is difficult to intubate or to ventilate by alternate techniques. A cricothyroidotomy is performed by the insertion of a large-bore (12- to 14-gauge) catheter-over-needle through the cricothyroid membrane. The catheter is then advanced and attached to a 50-psi oxygen source for transtracheal catheter jet ventilation.7 Guidelines for acceptable transtracheal jet ventilation systems have been outlined by Benumof and Scheller. 25 A tracheotomy is indicated when severe anatomic deformities or maxillofacial or laryngeal trauma preclude the use of nasotracheal or orotracheal routes for intubationJ7 The tracheotomy is usually performed in the controlled setting of an operating room only after the airway has been controlled with the described

techniques. It is not the best airway management technique in an acute setting] Endotracheal intubation is then confirmed by auscultation of bilateral breath sounds, by chest expansion with ventilation, by the absence of epigastric sounds, and by the confirmation of end-tidal carbon dioxide (ETc02) with a CO2 detector (ie, mass spectrometer, infrared or colorimetric detector).26 A multicenter study recently investigated the use of ETc02 measurement in confirming endotracheal tube placement. 27 Omato et a127 concluded that in both the nonarrested and the arrested patient an ET¢02 measurement greater tha n 0.5% for more than six breaths confirmed the endotracheal tube placement in the airway of the

Fig 2. Esophageal tracheal combitube.

CURRENT CONCEPTS IN CARDIOPULMONARY RESUSCITATION

393

Fig 3. Syringe esophageal detection device,

patient. 27 A low ETc02 measurement in a nonarrested patient confirmed misplacement of the endotracheal tube. In the setting of cardiac arrest, a low ETc02 may not be caused by tube malposition but may result from a low blood flow state, poor ventilation (eg, airway obstruction), severe ventilation/perfusi0n mismatch (eg, massive pulmonary embolism), and exogenous epinephrine administration. The Wee esophagus detector is a 60-mL syringe-like device that can be attached to an airway (Fig 3). Fifty milliliters is initially injected into the endotracheal tube. The lack of resistance to the aspiration of air indicates an endotracheal intubation. Resistance occurs with esophageal intubations.28 Once the airway has been established and confirmed, ventilation may be achieved by a variety of techniques, including an anesthesia bag, a self-inflatingbag, an oxygen-powered demand valve, or an au.tomatic transport ventilator (ATV). Except for the ATV, the tidal volumes of each breath may vary.7 CIRCULATION AND PERFUSION

The perfusion of vital organs with oxygenated blood during CPR is accomplished by closed chest compressions. The cardiac output (20% of normal) and cerebral perfusion (10% to 20%) are markedly reduced during cardiac arrest and CPR when compared with spontaneous circulation. 29 The emphasis of CPR research has been to improve on CPR perfusion with different compression techniques. The current AHA guidelines in adult CPR recommended a rate of 80 to 100 per minute, a depth of 1.5 to 2 inches, and a compression-to-relaxation ratio Qf 50:50. 7 Adequate comPressions are confirmed with palpable carotid or femoral artery pulses. However, palpable pulses with compressions do not affirm the adequacy of CPR, which is discussed later. Since the inception of CPR in the 1960s, numerous investigations have focused on the mechanism of blood flow during closed chest compression. Controversy exists over this mechanism. Most of the controversy has centered around two mechanisms of blood flow: the cardiac pump and the thoracic pump"3° If the cardiac pump is operative, compression of the heart between the sternum and the spine and vertebrae results in the forward ejection of blood from the heart. During the compression phase of CpR, the mitral and tricuspid valves close while the aortic and pulmonic valves open, causing forward flow. The

right and left ventricle are compressed during this phase (Fig 4). 29 During the relaxation phase of CPR, there is a decline in intracardiac pressure with subsequent opening of the mitral and tricuspid valves, causing the heart to fill with blood. Several transesophageal echocardiographic studies support the above mechanism.3~-33 In the 1960s, hypotension during coronary angiography was commonly treated by having the patient cough. The increase in intrathoracic pressure was believed to be transmitted to the aorta, increasing diastolic pressure and coronary perfusion to wash out the radiopaque dye. "Cough CPR" has been noted in several reports to maintain consciousness in patients in ventricular fibrillation for as long as 100 secondsY-36 The thoracic pump theory arose from these observations. During the compression phase of CPR, an increase in intrathoracic pressure causes venous collapse at the thoracic inlet while the intrathoracic arterial vessels become pressurized. The pressure difference between the intrathoracic arterial vessels, the peripheral arterial tree, and the venous system allows for the forward flow of blood. With this theory, the heart is a passive conduit for blood flow. This unequal transmission of pressures between the arterial and venous system was observed experimentally in dogs during CPRS Another study showed forward flow of blood in dogs during CPR without significant changes in left ventricular size during both compression and relaxation phases of chest compression, further supporting this theoryY Recent investigations suggest that spontaneous gasping during cardiac arrest is associated with gas exchange and forward blood flow.39,4° Gasping is a short, vigorous insPiratory effort controlled from medullary centers only after disruption of inhibitory control from the pons. Brainstem transections and progressive brainstem anoxia have been shown to disable pontine pneumotaxic control and produce gasping. 41,42Rodents that were intubated but not ventilated, electrically induced into ventricular fibrillation, and given precordial compression after 4 minutes showed pulmonary gas exchange with gasping. Higher PaO2 and lower Paco2 were noted with higher gasping rates. Better resuscitation rates were shown with rodents that maintained spontaneous gasping during precordial compression. Another study using the porcine cardiac arrest model showed that pressure gradients generated during the inspiratory and expiratory phases of a gasp could provide forward blood flow. In the inspiratory phase, the negative intrathoracic pressure

394

TORRES AND WHITE

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would cause a decrease in aortic pressure to below that of fight atrial pressure. This would cause blood flow from the right to t!ae left side of the heart. In the expiratory phase, this gradient is reversed, and coronary perfusion pressure increases.43 During the early phase of CPR, spontaneous gasping provides a mechanism of ga s exchange and circulation. The effect of spontaneous gasping on the outcome of CPR is yet to be investigated. Alternative compression techniques have been proposed in an attempt to improve perfusion during CPR. One such technique is the interposed abdominal counterpulsation (IAC CPR) initially described in 1976. 44 With this method of CPR, the abdomen is compressed.4s Improvedcerebral blood flOW,46 carotid blood flow, 47 and end-diastolic artefiovenous pressure difference48 have been observed experimentally with IAC CPR Versus standard CPR, but clinical studies show conflicting results. In a prospective study of 103 in-hospital patients undergoing either IAC CPR or standard CPR, the return of spontaneous circulation was more frequent with IAC CPR (51%) than with standard CPR (27%)i A higher survival to hospital discharge wa s noted with the IAC CPR 25% versus standard CPR 7%. 49 Another prospective study of 143 patients with asysto!e or electrical mechanical dissociation showed improved immediate 24-h0ur surviva! rates of 48% (IAC CpR) versus 28% (standard CPR). However, in this same Study, no patients from either group survived to hospital discharge.5° Further clinical investigations are warranted to confirm the efficacy of thi s alternative technique. The active compression-decompression CPR (ACD CPR) techniqu e was formulated on the basis of an anecdotal case report of successful CPR with the use of a toilet plunger, sf An

Fig 4. A schematic diagram of hemodynamics during CPR. (A) The cardiac pump theory. (B) Thoracic pump theory. See text for exPlanation. (From KQhn et al, 31with permission.)

ACD CPR device was int.roduced in 1992 (Fig 5). 52 This hand-held device is capable of active compression and active decompression of the chest. The ACD device contains a silicone rubber suction cup, a central piston or bellows, and an area of compression within the bellows. Animal models have shown improved perfusi0n of the brain, heart, and kidneys with ACD CPR compared with standard CPR.53,54 Improved hemodynamics with ACD CPR have been shown in several studies. 51,53 Increased end-tidal carbon dioxide concentration femoral systolic pressures, and improved acid-base status were noted with ACD CPR during a Prospective crossover in adult cardiac arrest patients. This suggests that ACD CPR may improve hemodynamics over standard CPRY Two in-hospital cardiac arrest studies noted a twofold improvement in the rate of return of spontaneous circulation and 24-hour survival.51,56A recent prospective, controlled trial randomized preh0spital nontraumatic cardiac arrest to ACD CPR (26 patients) and standard CPR (30 Patients). No improvement was noted in the rate of regaining spontaneous circulation (38.5% v 40%) or rate of hospital discharge (11.5% v 13.3%) between ACD CPR and standard CPR patients, respectively.57 Although these new CPR compression techniques may appear to be promising, further evaluation is necessary before modifying the current AHA-recommended CPR guidelines. Potentially, both the cardiac pump and the thoracic pump mechanisms may contribute to blood flow during CPR. The predominant mechanism may depend On anatomic or pathophysiological variations in a patient receiving CPR. These theories are likely to be useful in the evolution of newer compression techniques, until the clinical relevance of the theories and

CURRENT CONCEPTS IN CARDIOPULMONARY RESUSCITATION

395

Fig 5. The Active Compression-Decompression (ACD) device, (From Pellet al, 17~w i t h permission,)

techniques are established, current AHA CPR guidelines are recommended. MONITORING CPR PERFORMANCE

In the past, the effectiveness of CPR was assessed by palpation of carotid or femoral pulses and observation of pupillary size. These are very indirect indicators of perfusion and provide no indication of adequate cardiac output during CPR. Changes in pupillary size may be suggestive of resuscitation success and neurological outcome. 58 Persistently constricted or progressively constricting pupils may indicate a greater probability of successful CPR and favorable neurological outcome than persistently dilated or progressively dilating pupils (38% v 2%). 59 Pupillary dilatation also may result from the administration of adrenergic or anticholinergic drugs given during resuscitation. This may interfere with the interpretation of pupillary size during CPR. End-tidal carbon dioxide (ETc02) monitoring can be used as a guide to CPR effectiveness. 6°,61 With ventilation held constant, ETc02 correlates with lung perfusion and cardiac output. The alveolar partial pressure of carbon dioxide PACOainfluences the level of ETc02. The PAc02 is determined by the alveolar ventilation equation62: PACO2 = k × ~7co2/~/A = k × ~Qco2/'QE(1 - VD/VT)

where k is a constant, ~Zc02 is carbon dioxide excretion, VA is alveolar minute ventilation, VE is minute ventilation, and VD/VT is deadspace volume over tidal volume. By holding the denominator (ie, alveolar minute ventilation) constant, the PACO2 is determined by S)coa. Carbon dioxide excretion (Vc02) is thus influenced by carbon dioxide production and pulmonary blood flow or cardiac output. Several animal studies have shown a close correlation between ETc02 and changes in cardiac output. 61,63 A sudden increase in ETc02 is seen with return of spontaneous circulation in arrested humans. 64 Clinical studies indicate that ETc02 measurements during

CPR may be predictive of the resumption of spontaneous circulation. 65,66 The mean ETco2 in patients who developed a pulse after CPR was 19 +_ 14 (SD) mmHg, whereas those without spontaneous return of circulation had a mean ETc02 of 5 _+ 4 (SD) mmHg. 64 End-tidal carbon dioxide measurements may be a useful adjunct in monitoring the effectiveness of CPR. The usefulness of central venous oxygen saturation (Scvo2) has been reported in evaluating oxygenation and systemic circulation during CPR. 67 Central venous Oa saturation measured from the internal jugular vein has been shown to approximate mixed venous O2 saturation measured from the pulmonary artery. 6a In a cardiac arrest, central venous placement would be easier than pulmonary artery catheter placement. Central venous O2 saturation with an oxymetric central venous catheter and ETc02 monitoring was performed during CPR on a 54-year-old man with a history of mitral stenosis and aortic insufficiency. 67 After 35 minutes of ACLS, there was a restoration of spontaneous circulation. Figure 6 shows the changes in both ETco2 and Scvo2 during the resuscitation. This case report suggests that Scvo2 monitoring may be advantageous by providing information on tissue oxygenation. Assessing the effectiveness of CPR can be achieved in several ways. These include direct arterial blood pressure measurements, 69 arterial blood gas analysis, venous blood gas analysis, 7° end-tidal carbon dioxide monitoring, and possibly central venous oxygen saturation. ADVANCED CARDIAC LIFE SUPPORT (ACLS) The administration of BLS to a cardiopulmonary arrest

patient is only a temporizing measure until more definitive therapy, ACLS, can be applied. Survival greatly depends on the speed of delivery of BLS and ACLS. 71,72 Provision of BLS within 4 minutes and ACLS within 8 minutes is associated with a survival rate as high as 43%. 7 Immediate recognition and treatment of potentially life-threatening arrhythmias is an essential aspect of ACLS. Assessment of the hemodynamic

396

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impact of an arrhythmia determines the aggressiveness of the therapy pursued. "Treating the monitor" may result in the deterioration of a previously stable situation.73 The unstable, hypotensive, pulseless, or unconscious patient requires immediate electrical cardioversion, whether the arrhythmia is supraventricular or ventricular in origin. In the stable patient, it is important to avoid acting on a perceived arrhythmia. Electrocardiogram artifacts must be ruled out, because attempts of cardioversion in this setting may lead to ventricular fibrillation. Documentation and scrutinization of the arrhythmia in the stable patient will provide better treatment strategies. B RADYARRHYTH M IA

Definition and Cause A heart rate of less than 60 beats/min defines bradycardia. However, bradycardia may be absolute and relative. 8 An "absolute" bradycardia can be seen in well-conditioned athletes as a normal baseline heart rate. A decrease from the normal baseline heart rate is known as a "relative" bradycardia and may be associated with symptoms. The causes of bradycardia can be separated into reversible and irreversible. Reversible causes include myocardial ischemia, hypoxemia, electrolyte abnormalities (eg, hyperkalemia), medications, decreased sympathetic tone (eg, high spinal anesthesia74), and increased vagal tone. The irreversible causes include (1) acquired types from myocardial infarction, postcardiac surgery, bacterial endocarditis, connective tissue disease, infiltrative diseases of the heart (amyloidosis, hemochromatosis, etc.), muscular dystrophy, and hypertensive heart disease; and (2) congenital types. 75 Supraventricular bradyarrhythmias can be categorized into disorders of impulse formation or of impulse conduction. Sinus bradycardia, sinus pause or arrest, and sick sinus syndrome are disorders of impulse formation. These disorders are caused by a disturbance in the rate of phase 4 depolarization of cardiac pacemaker cells. First-degree, second-degree (types I and II), advanced, and complete heart block constitute disorders of impulse conduction. The further

distal the heart block becomes, the more danger for electrophysiological deterioration attributable to a less reliable escape mechanism.

Treatment The development of hypotension, chest pain, or shortness of breath during bradycardia of any type (symptomatic bradycardia) should be treated with atropine sulfate, 0.5 to 1.0 mg intravenously (IV) or 2 to 2.5 times the IV dose in 10 mL saline or sterile water administered endotracheally,76 unless the 10 mL of saline is administered after the dose of atropine. This may be repeated as needed at 3- to 5-minute intervals to 0.04 mg/kg. 77 Alternative therapies include external transcutaneous, transesophageal, or transvenous pacing, dopamine infusion at 5 to 20 pg/kg/min, or epinephrine infusion at 2 to 10 ~g/min. The use of these interventions has diminished the use of isoproterenol. Isoproterenol can be harmful by increasing myocardial oxygen demand ([31 effect) and decreasing systemic vascular resistance ([32 effect). Figure 7 is the AHA algorithm for the treatment of bradyarrhythmias.

SUPRAVENTRICULAR TACHYARRHYTHMIAS

Cause The supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, atrioventricular (AV) nodal reentrant tachycardia, multifocal atrial tachycardia, AV reentrant tachycardias, and other less common tachyarrhythmias. The mechanisms of tachycardia include reentry, abnormal automaticity, and triggered activity. Reentry is the most common cause of tachyarrhythmias including atrial flutter, AV nodal tachycardia and AV reentry tachycardia with accessory pathways. 72 The supraventricular tachyarrhythmias that often require emergent medical attention include paroxysmal supraventricular tachycardia (PSVT) with severe hypotension and atrial fibrillation or flutter with rapid ventricular response.

CURRENT CONCEPTS IN C A R D I O P U L M O N A R Y

• Assess ABCs • Secure airway • Administeroxygen • Start IV = Attach monitor, pulse oximeter, and automatic sphygmomanometer

• • • • •

RESUSCITATION

397

by slowing conduction and prolonging the refractory period. Adenosine is effective in terminating PSVT, because PSVT is most commonly caused by reentry in the AV node. sl-s3 The transient AV block produced by adenosine may be useful in diagnosing the underlying rhythm, 84-s6 as illustrated in Fig 9. The drug must be injected rapidly and near the central circulation because of its rapid cellular uptake and metabolism. The half-life of adenosine is less than 5 seconds. If the first dose is unsuccessful, a second dose of 12 mg can be administered after 1 to 2 minutes. Methylxanthines antagonize the effects of adenosine on the AV node, and therefore a 9-rag starting dose may be needed. Dipyridamole potentiates the effects of adenosine, and therefore a starting dose of 1.5 to 3 mg is used. s7 Carbamazipine can itself impair AV conduction, and therefore lower doses of adenosine (as with dipyridamole)) should be used in this circumstance. Recurrent or persistent PSVT can be treated with verapamil, 5 mg IV, and a repeat dose of 5 to 10 mg may be given, if needed, in 15 to 30 minutes after the initial dose. Rate control of atrial fibrillation and atrial flutter can be achieved with verapamil. 8s Verapamil or other AV nodal blocking agents should be avoided in patients with Wofff-Parkinson-White syndrome who develop atrial fibrillation or flutter. AV nodal blockade can increase conduction through the accessory pathway, causing acceleration of ventricular rate and possible ventricular fibrillation.

Assess vital signs Review history Perform physical examination Order 12-lead ECG Order portable chest roentgenogram

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Intervention sequence • Atropine 0.5-1.0 mg :l:§ (I & lid) • TCP, if available (I) •/~ine 5-20 pg/kg per min (lib) • Epinephrine 2-10 pg per min (lib) • Isoproterenol¶

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*Serious signsor symptoms must be related to the slow rate. Clinical manifestations include: symptoms (chest pain, shortnessof breath, decreased level of conaouanass) and skjns (low BP, shock, pulmonaryc o ~ , CHF, acute MI). "t'Do not delay TCP while awa~ng IV access or for =rrop/ne to take effect if patient is sympfomabc. ~:Denervated transplantedhearts will not respondto ~roll~ne.Go at once to pacing, catecho/amine inlusian, or bo~. §Ab'op/ne shouldbe given in repeat doses in 3-5 min up to total of 0.04 mg/kg. Consider shorter d ~ n g intervals in severe clinical conditions. It has been suggestedthat atropine shouldbe used with caution in aMoventTk:;ular(AV) block at the His-PurkJnjelevel (type li AV blod< and new third-degree block wi~ wide QRS complexes) (Class llb). IINever treat thin, degree heart block plus venthcular escape

VENTRICULAR

BRADYARRHYTHMIAS

Ventricular bradyarrhythmias arise from complete heart block with a slow idioventricular escape rhythm of 15 to 30 beats/rain. Rapid treatment is mandatory in most patients. Treatment includes atropine initially as previously discussed followed by transcutaneous or transvenous pacing.

beats w ~ lidocaine.

¶/sopro~e~eno/should be used, if at all, with exteme cau~don. At Iow dosas itis Classlib (possiblyhelpful);at higherdoses it is Class III (harmful). #Verify patient tolerance and mechanical capture. Use analges~ and sedation as needed.

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Cause

Fig 7. Bradycardia algorithm. Abbreviation: TCP, transcutaneous pacing. (From the American Heart Association, 76 with permission.)

The ventricular tachyarrhythmias include ventricular premature depolarizations, ventricular tachycardia (VT), and torsades de pointes, an atypical form of VT. Hypoxemia, hypercarbia, hypokalemia, hypomagnesemia, digitalis toxicity, and acidbase disorders are reversible causes of ventricular ectopy. These causes must be ruled out in a timely fashion before initiating pharmacological therapy.

Treatment An example of PSVT is depicted in Fig 8. If PSVT presents with hemodynamic instability the therapy of choice is cardioversion with 50 J. Cardioversion with 100, 200, 300, and 360 J may be repeated if necessary. If the patient is hemodynamically stable, vagal maneuvers such as carotid sinus massage or the Valsalva maneuver may be employed. Termination of this tachyarrhythmia can be accomplished with 6 mg of adenosine given rapidly through an antecubital or central vein. 7H° Adenosine acts on the AV node

Treatment The treatment of VT depends on the hemodynamic effects of the tachycardia on the patient. An unstable patient with hypotension, pulmonary edema, or clinical or electrocardio-

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Fig 9. A supraventricular tachycardia of uncertain origin at a rate of 150 beats/rain. After the administration of adenosine, 6 mg, atrial flutter waves become evident.

graphic (ECG) changes of myocardial ischemia or infarction is managed with cardioversion. Incremental energy doses of 100, 200, 300, and 360 J are used until the VT is terminated. The AHA algorithm for symptomatic tachyarrhythmias, including supraventricular tachycardia and VT, is outlined in Fig 10. In the stable patient, VT is treated initially with 1.0 to 1.5 mg/kg of IV lidocaine. Repeat doses of 0.5 to 0.75 mg/kg are administered every 5 to 10 minutes, until the VT is resolved or a total of 3 mg/kg is reached. If no resolution occurs with lidocaine, procainamide is administered at a rate of 20 to 30 mg/min IV until the VT is terminated or a total dose of 17 mg/kg is given. Constant blood pressure and ECG monitoring are mandatory because significant hypotension and QRS widening I Tachycardia with serious signs and symptoms related to the tachycardia

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*Effective regimens have included a sedative (eg, diazepam,

midazolam, barbiturates, etomidate, ketamine, methohexital) with

or without an analgesic agent (eg, fentanyl, morphine, meperidine). Many experts recommend anesthesia if service is readily available. 1Note possible need to resynchrenize after each cardioversion. ~:lf delays in synchronization occur and clinical conditions are critical, go to immediate unsynchronized shocks. §Treat polymorphic VT (irregular form and rate) like VF: 200 J, 200-300 J, 360 J. IIPSV-F and atrial flutter often respond to lower energy levels (start with 50 J). Fig 10. Algorithm for symptomatic tachyarrhythmias. (From the American Heart Association, TM with permission.)

can occur with procainamide administration. Failure to terminate VT with this therapy would lead to the use of bretylium in a dose of 5 to 10 mg/kg over 8 to 10 minutes. 89 Repeat doses of 5 to 10 mg/kg may be given every 5 minutes until a total dose of 30 mg/kg is given. 76 If the VT fails to resolve with the outlined therapy, synchronized cardioversion should be implemented. Torsades de pointes, which means "twisting of the points," is an atypical form of VT. 90,91This tachyarrhythmia has a polymorphous appearance resulting from the QRS axis twisting around a baseline. The primary electrophysiological mechanism in this tachyarrhythmia is the marked and nonuniform delay in repolarization, which is noted as a prolongation of the QT interval (greater than 0.44 seconds) on the ECG. The QT prolongation can be acquired or congenital in origin. Acquired QT prolongation is associated with drugs (procainamide, disopyramide, quinidine, phenothiazines, lithium, tricyclic antidepressant, diuretics, astemizole, terfenidine, etc.), electrolyte abnormalities (hypokalemia and hypomagnesemia), myocardial ischemia or infarction,92 and right radical neck dissection93 or stellate ganglion block. Congenital QT prolongation is seen with Jervell-Lange-Nielsen (associated with congenital neural deafness) and Romano-Ward syndromes. 94 Pleomorphic (or polymorphous) ventricular tachycardia (PVT) (Fig 11) is similar to torsades de pointes. Some categorize PVT separately from torsades based on a normal QT interval. Others include torsades as a type of PVT. 95-98The presence or absence of QT prolongation directs the therapy of "torsades de pointes" or PVT, respectively. In the presence of QT prolongation, therapy is aimed at reducing the repolarization time. This includes discontinuing the medications listed, correcting electrolyte abnormalities, and increasing the heart rate (atrial or ventricular overdrive pacing). Torsades has been effectively treated with magnesium sulfate. Some recommended it as the first line of therapy in unstable torsades. 99:°° In the absence of QT prolongation, therapy for VT may be used. Magnesium sulfate also may be used in this circumstance. Defibrillation should be used if PVT deteriorates hemodynamically. The AHA algorithm for tachyarrhythmia management is outlined in Fig 12. This algorithm avoids the use of verapamil in wide complex tachycardia of indeterminate origin. Verapamil given in the setting of VT can cause severe hypotension and

CURRENT CONCEPTS IN CARDIOPULMONARY RESUSCITATION

399

~ | ! II FI2t:I:|t-2~,.~t:|if4|g,It N]:[::~rN I~:N~Flg;|Tt:II~:IT;~tl1:1~tl~l;lt 1~:~ri:~g t~t] t ~:~-I~-l/_ ~rd 11Ltt t~t I II ! i i :. i t i.: lit ~-t~ ;tlL~.;~.~!..-P2..~ :tl3g11~-~:~:~-l~t~-;~'l;;:',-:;!:~~:~:iif i: i?tliglt.. ff : : ; .'4: i t~ i; -; I' ~ :Ill tt .| :~

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cardiovascular collapse. Cardioversion is the therapy of choice if the patient becomes unstable. PULSELESS VENTRICULAR VENTRICULAR

TACHYCARDIA

electrical energy units used for the defibrillator shock is measured in joules (J) or watt-seconds (W. s). Energy (J) = Potential difference (V) × Current (Amp) × Time (s)

OR

FIBRILLATION

The maximum energy output from a defibrillator available in the United States is 360 J delivered into a 50-ohm load. This is the standard impedance used by defibrillator manufacturers to calibrate energy output. The delivery of a successful defibrillatory shock in VF is dependent on the energy output of the defibrillator1°4 and the resistance to current flow during defibrillation. A daily defibrillato r checkl including pacemaker function available in some units, is highly recommended to assure proper function. Resuscitation carts should also be checked for supplies regularly. Maintenance guidelines for defibrillators are available. ~°5 The transthoracic current flow during defibrillation is inversely related to the resistancem4; for this purpose sterilizable defibrillator testing devices are available for testing defibrillators with internal paddles, as in cardiac operating rooms (The Flasher; Solid State Sonics and Electronics, Inc, Topeka, KS). These can

Therapeutically, pulse!es s ventricular tachycardia (PVT) and ventricular fibrillation (VF) may be considered as similar entities requiring the same treatments. These arrhythmias are the most common form of cardiac arrest and are the most treatable, yielding the greatest likelihood of immediate and long-term survival, both in-hospital and out-of-hospital.l°~ This observation has led to the application of early defibrillation in out-of-hospital settings with automated external defibrillators, which may be operated by basic emergency medical technicians or first responders with minimal training. Many patients at risk of recurrent cardiac arrest from V F or symptomatic ventricular tachycardia are now managed with implantable cardiac defibrillators 1°2,1°3 that provide several treatment options, including antitachycardia and antibradycardia pacing, synchronized Cardioversion, and defibrillation. Early defibrillation is the definitive therapy for VE The

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Fig 12. Tachycardia algor!thm. (From the American Heart Association, TM with permission.)

tCapotidsinus pressure is cormaJndicatedin pa~ents~ ~ bruits,avoidlee t,mwr immersioninpatientsW~l ischemichec't aisease. ~ff the wide-Corn@ex tachyca dia is knownwith certainty to be PSVTand BP is normaVelevated,sequence can include~

400

be used at the beginning of each operation to assure an intact defibrillator energy discharge circuit. Proper electrode placement, firm pressure against each paddle ~11 kg/paddle), optimal electrode-chest wall contact with electrode paste or selfadhesive electrode pads,l°4 and defibrillation at end-expiration 1°6 serve to minimize impedance during defibrillation. During a witnessed, unmonitored cardiac arrest, a single precordial thump may be delivered before beginning CPR while waiting for a monitor-defibrillator to become available. During a witnessed, monitored cardiac arrest with either pulseless VT or VF present, immediate defibrillation with 200 J should be delivered if a defibrillator is readily available. If this is Unsuccessful, a second shock of 200 to 300 J, and, if necessary, a third shock of 360 J should be administered in rapid succession. If pulseless VT or VF is unresponsive to this initial intervention, pharmacological intervention becomes necessary. IV access should be established as early as possible. Central IV access provides more rapid drug delivery and higher arterial drug levels than injections into peripheral veins. The use of glucose-containing fluids during resuscitation should be restricted to patients who are hypoglycemic. There is evidence that hyperglycemia in the setting of global cerebral ischemia can worsen neurological outcome m cardiac arrest survivors. ~°7-1°9 This was initially noted in 1977 by Myers and Yamaguchi H° in animals receiving dextrose-containing solutions during resuscitation. In the setting of global cerebral ischemia, hyperglycemia is believed to increase lactic acid production through anaerobic metabolism that leads to adverse neurological outcome, m Lactated Ringer's or normal saline should be used during cardiac resuscitation. Drug therapy for pulseless VT or VF starts with epinephrine. An intravenous dose of 1.0 mg ( 10 mL of a 1:10.000 dilution) or 2 to 2.5 mg endotracheally followed by 10 mL of normal saline is the recommended starting dose of epinephrine. This dose ( 1.0 rag) should be repeated every 3 to 5 minutes for the duration of the cardiac arrest. The clinical benefits of epinephrine during cardiac arrest are based on the increase in cerebral and coronary blood flow.112,113Epinephrine causes vasoconstriction in noncritical tissue beds, prevents arterial collapse, and diverts blood flow tO the heart and brain. Phenylephrine or Other alpha-agonists have not been shown experimentally to be more effective or less injurious than epinephrine, and therefore epinephrine remains the initial drug of choice. Alternative dosage regimens for IV epinephrine include an intermediate dose (2 to 5 mg), escalating dose (1 mg, 3 mg, 5 mg), and high-dose (0.1 to 0.2 mg/kg) every 3 to 5 minutes. If an initial trial of standard-dose epinephrine is not effective, these alternative epinephrine doses are considered acceptable and possibly helpful. Early reports suggested that higher epinephrine doses may improve resuscitation outcome by elevation of coronary perfusion pressure, u4 Some studies have shown an improvement in the rate of spontaneous circulation with the use of high-dose epinephrine when compared with standard-dose epinephrine. H5,116 No study has shown an improvement in survival to discharge with high-dose epinephrine.ll7,118 After the initial dose of epinephrine, the fourth defibrillatory shock of 360 J Should be delivered. If internal shocks are being

TORRES AND WHITE

delivered, the 50-J setting would be approximately equivalent to the 360-J external shock. Persistent pulseless VT or VF is treated with an antifibrillatory drug, lidocaine. The pharmacological actions of lidocaine include decreased ventricular automaticity, 119 suppression of reentrant circuits because of boundary currents in acute ischemia, 12° suppression of reentrant excitation by inducing complete block in reentrant pathways, t2~ and elevation of VF threshold.122 The initial dose of lidocaine is 1.5 mg/kg IV or through the endotracheal tube. No data are available on the absorption of lidocaine from the tracheobronchial tree during cardiac arrest. After the initial lidocaine bolus, a defibrillatory shock of 360 J is delivered. A repeat dose of 1.5 mg/kg may be repeated in 3 to 5 minutes, to a total dose of 3.0 mg/kg. If lidocaine fails to terminate pulseless VT or VE bretylium can be used. The antiarrhythmic mechanism of bretylium remains unclear. It may be attributable to the prolongation of the action potential duration, thereby facilitating the termination of reentrant activity. 123 The alternative mechanism of action may be caused by its initial sympathomimetic effect from the release of norepinephrine by the adrenergic nerve endings. 124,125 This may improve conduction and thus reduce the opportunity for sustaining reentrant circuits during ischemia. Bretylium also increases VF threshold. The initial dose is 5 mg/kg, followed by a 360-J shock. If this is unsuccessful, a second dose of 10 mg/kg can be administered, followed by a shock. If needed, a third dose of 10 mg/kg can be repeated, followed by another shock. One adverse effect of bretyliUm is supine hypotension, which may occur 15 to 20 minutes after an injection. This is attributable to a sympatholytic effect of bretylium with a decrease in norepinephrine release by the sympathetic nervous system. This hypotension can be severe.l~6 The correction of electrolyte abnormalities such as hyperkalemia, hypokalemia, or hypomagnesemia may allow defibrillatory shocks to restore spontaneous circulation. The role of magnesium in the maintenance of stable cardiac rhythm is supported by several studies.127 -129 Normal serum magnesium levels may not indicate adequate magnesium levels at the tissue level. 13° In the setting of refractory pulseless VT or VF, hypomagnesemia should be considered and treated with 1 to 2 g of magnesium sulfate over 1 to 2 minutes. 131 Procainamide, 30 mg/min to a total of 17 mg/kg, also may be used to treat refractory VT or VE The recommendations for the use of sodium bicarbonate during cardiac arrest have changed. In cardiac arrest, the use of sodium bicarbonate (NaHCO3) should be limited to preexisting metabolic acidosis, severe documented metabolic acidosis, or hyperkalemia, and only if the above-outlined therapeutic interventions have been unsuccessfu !. Previously, NaHCO3 had been used early and frequently during cardiac arrest. Some Studies continue to support the early use of NaHCO3132,133 in CPR. However, the early administration of NaHCO3 in cardiac arrest has been shown not to improve survival. 134,135 Numerous adverse effects have been noted with the use of NaHCO3, including severe plasma hyperosmolality] 36 paradoxical cerebrospinal fluid acidosis] 37 carbon dioxide generation with subsequent increase of tissue acidosis, 138 and coronary perfusion pressure reduction when administered without epineph-

CURRENT CONCEPTS IN CARDIOPULMONARY RESUSCITATION

rine. 139,140If used, the initial dose is 1 mEq/kg. A 0.5-mEq/kg dose may be repeated at 10-minute intervals or as directed by arterial blood gas and base deficit determinations. The AHA algorithm for the treatment of pulseless VT and VF is illustrated in Fig 13. PULSELESS ELECTRICAL ACTIVITY (PEA) AND ASYSTOLE

Pulseless electrical activity (PEA) is a group of cardiac arrhythmias characterized by pulselessness in the presence of some kind of electrical rhythm other than VT or VF. Electromechanical dissociation (EMD), idioventricular rhythms, ventricular escape rhythms, postdefibrillation idioventricular rhythms, bradY-asystole, and "pseudo-EMD" are included in this designation of PEA. The therapy of PEA is directed toward the identification and coi'rection of the underlying cause, including hypovolemia, hypoxemia, cardiac tamponade, tension pneumothorax, hypothermia, massive pulmonary embolism, drug overdosage, hyperkalemia, metabolic acidosis, and acute myocardial infarction. Epinephrine is used to maintain perfusion pressure to vital organs during CPR while immediate diagnostic assessment and disorder-specific therapy is initiated. For example, arrhythmias caused by calcium-channel blockade overdose 1~1 or hyperkalemia i42 may be treated with intravenous calcium. Figure 14 outlines the AHA algorithm for PEA. Asystole is typically an irreversible and terminal event. This form of cardiac arrest results from severe hypoxemia, hyperkalemia, massive myocardial infarction, drug overdose, metabolic acidosis, and hyp0thermia. Brief intervention may be warranted in some patients with potentially reversible causes such as hypothermia, acidosis, or hyperkalemia. Temporary pacing has

401

not been shown to improve outcome from asystole. Figure 15 is the AHA algorithm for asystole. INCIDENCE AND OUTCOMES OF ANESTHESIA-RELATED CARDIAC ARREST

The incidence of anesthesia-related cardiac arrest in the operating room ranges from 0.5 to 9.4 cases per 10,000 anesthetics. 143 153Keenan and Boyan 147reported an incidence of 1.7 anesthesia-related cardiac arrest per 10,000 anesthetics over a 15-year period, with a mortality rate of 0.9 cases per 10,000 anesthetics. In a later study, Keenan and Boyan 152 showed a decrease in anesthetic cardiac arrest from 2.1 arrests per 10,000 cases (during 1969 to 1978) to 1.0 arrest per 10,000 cases (during 1979 to 1988): 152This impiovement was attributed to a decrease in preventable respiratory events because of improved intraoperative monitoring such as pulse oximetry, capnometry, and disconnection alarms. Several reviews noted that most operating room cardiac arrests were related to the patient's underlying disease or surgical factors such as uncontrolled hemorrhage.147 150-152 The main causes for anesthesia-related cardiac arrest included relative or absolute anesthesia overdose with or without hypovolemia, hypoxemia, and multifactorial cause. 147,15°,152Anesthesia-related cardiac arrest occurred commonly within 30 minutes of induction.148,15o,ls! The risk for anesthetic cardiac arrest was increased in the pediatric agegroup 149 (threefold increase over adults), 15° the elderly, 149,15I patients with ASA physical status above class 3,143'147'149 and emergency cases (sixfold increase over elective cases).15° The frequencY of anesthesia-attributable deaths in the operating room ranged from 0.i tO 6.1 per 10,000 anesthetics, m-153 Discharge survival rates from an anesthesia-related cardiac

• ABCs • Perform CPR until defibrillator attached* • VFNT present on defibdllator

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Fig 13. A l g o r i t h m permission.)

for ventricular

fibrillation

/ ]

¶ • Lidoeaine 1.5 mg/kg IV push. Repeat Class I: definitely helpful in 3-5 min to total Loading dose of Class lie: acceptable, probably help~l 3 rng/kg; then use Class lib: acceptable, possibly helpful • B r e ~ l u m 5 rog/kg IV push. Repeat in Class Ut: net indk:ated, may be hean~l 5 rain at 10 m~;~kg *Precordial thump is ~i Cla,~ lib actiea in • l i ~ g n e ~ u m sulfa~ 1-2 g IV in witnessed arrest, no pulse, and no tots•dee de pointes or suspected defibrillator immediately available. hypomagnseamic state or severe tHypo~ermis cardiac arrest is treated refractory VF differently after this point. See • Procairmmide 30 mg/rein in retractor/ on hypothermia. VF (maximum total 17 rog~g) :~The recommended dose of ep/r/ephrine # • Sodium b/carbonete (1 mEql~g IV): is 1 mcj IV push every 3-5 rnin. If this Class Ila approach falls, several Class lib dosing • if known preaxi~ng bioarbenateregimens can be considered: responave acidosis • Intermediate: epinephrine2-5 mg IV • if overdose with t~yctic push, every 3-5 min an~depraseants • Esc~ating:ep/nep//r/ne1 rag-3 rag• to alkalinize the urine in drug 5 mg iV push (3 rain apart) overdoses • High: ep/nephr/ne 0.1 mg/kg IV push, Class lib every3-5 min • if intubeted and co~nead long arrest § Sodium bicarbonate (t mEq/kg) is interval Class I if patient has known preexisting • upon ratum of spontaneous drculat~on hyperkalemia after long arrest interval I/Multtple sequenced shocks (200,1,200-300J, Class III 360 J) are acceptable here (Crass I), • hypoxic lac~o acidosis es~cially when medications are delayed

and pulseless ventricular tachycardia ( V F / V T ) .

( F r o m t h e American Heart Association, 76 w i t h

402

TORRESAND WHITE PEA includes

• Electr0mechenicat dissociation (EMD)

* Pseutto+EMD • Idioventricular rhythms • Ventricular escape rhythms • Bradyasystolic rhythms + Postdefibdllation idioventricular rhythms • Continue CPR • Intubata at once

• Obtain IV access • Assess blcx:x:l flow using Doppler ultrasound

! Consider possible causes (Parentheses=possible therapies and treatments) • Hypovolemia (volume infusion) • Hypoxia (ventilation) • Cardiac tamponade (pericardiocentesis) . • Tension pneumothorax (needle decompression) • Hypothermia • Massive pulmonary erndolism (surgery, throrabolytics) • Drug overdoses such as tdcycliss, digitalis, ~-blockers, calcium channel blockers • Hyperkalemia* • Acidosist • Massive acute myocardial inferction

1 •

Epinephrine

1 mg IV push, *:[: repeat every 3-5 rain

t

CEREBRAL PROTECTIONAND REsusCITATION

• If absolute bradycardia (<60 beats/mirl) or relative bradycardia, give atropine 1 mg IV . • Repeat evew 3-5 rain up to a total of 0.04 mg/kg§

Class h definitely helpful Class Ita: aocegtable, p r o l ~ help~l Class lib: acseptable, pustule/helpful Class II1:not indicated, may be harmful *S~d/um ~ 1 mEoWs is Clsss I if paUe~ hss known prsexis'dng hypedmmnm, "i'Sodlum b / ~ 1 mEo/kg: Ila

=, if known preexisting b i c a r b o ~

arrest resuscitation has not shown improvement in clinical outcomes. 155,158In Martens et al's 155 study, 11 out-of-hospital and five in-hospital patients sustained a witnessed cardiac arrest and were unresponsive to ACLS protocols for at least 10 minutes. Within 60 to 180 minutes of the onset of cardiac arrest, CPB was instituted by femoral vein and femoral artery cannulation as described by Shawl et al.159 Only 2 of these 16 patients (12.5%) lived to hospital discharge. Hartz et al158 reported a 12.5% survival rate of 32 outCof-hospital cardiac arrest patients who underwent CPB resuscitation. The current applications of CPB outside the operating room include selective CPB support during percutaneous transluminal coronary angioplasty. 16°,Ira Other applications Of CPB have been noted in the literatare. These ~nclude severe hypothermia, 162-164 massive pulmonary emboli, 156 hyperkalemic cardiac arrest, 165 and aortic valvuioplastyY6°

acidosis

+ if Ovemose wsh trieydic an'adeprssssnta • to alkalinize the urine in drug overdoses

Class lib e if intubatad and long arrest interval e upon mfurn of spontaneous d ~ after Iormj an'est inter~d . Class Ill • h,~.ooxiciaoUc eok:iosis *The rec~mrnended dose.o( ~ is I mg IV push avert,3.S min. Ifthis~Laprcaoh fails,several Class libdosing ~ can be ~de~ m l Intamiediata: ep/neptldtm 2-5 mg iV push. every 3-5 rain • Esca~ng: ep/neph#ne I mg-3 rng-5 mg IV push (3 rnin apart) • High: ep/nephr/ne 0.1 mg/kg IV push, every 3-5 rain § Shorter aOoplne dosirtg intervals are possibly helpful in cardiac anest (Class lib),

Fig 14. Algorithm for pulseless electrical activity (PEA). (From the American Heart Association,7swith permission.)

arrest varied from 36% to 75%. 142'144'i45'147'152'153Such a wide variation in discharge survival rates may be attributable to the different definitions for an "anesthesia-related" incident, different patient populations, and different data collection processes. Discharge survival rates for in-hospital cardiopulmonary resuscitation were found to be 16% in a Study by Ballew et al.~54 This study excluded patients resuscitated in the emergency room, operating room, recovery room, or cardiac catheterization laboratory. CARDIOPULMONARY BYPASS IN RESUSCITATION

The initial development of the cardiopulmonary bypass (CPB) machine had some basis in the field of resuscitation.155 In 1961, a patient with massive pulmonary embolism was stabilized with the use of CPB, underwent pulmonary artery embolectomy, and subsequently was discharged from the hospitalY 56 Although more widespread use Of CPB in resuscitation was suggested by May et al,~57 the primary use of CPB remained in the operating rooms during the 1970s and 1980s. The Use Of CPB in the in-hospital or out-of-hospital cardiac

Theterm "cardiopulmonary-cerebral resuscitation" or CPCR has been formulated to emphasize the need to preserve cerebral function and viability during a cardiac arrest situation. 166 Basic Life Support (BLS) is part of the "chain of survival ''167 that is integral to CPCR. BLS is successful when defibrillation or other definitive therapy can be delivered within 8 to 10 minutes of the onset of arrest.168 Beyond this timeframe, neurological damage may ensue. Several therapeutic efforts to reduce neurological damage during and after cardiac arrest have been investigated. Hypothermia has been shown in experimental models to have beneficial effects of reducing neural damage during ischemia only when it is introduced before, during, or immediately after the ischemic insult. 169,17° The clinical effect of hypothermia after ischemic neurological insult is unknown. Because moderate to deep hypothermia is associated with a number of potential complications, mild hypothermia 35.0°C to 37.5°C in the postischemic setting is recommended. 171 Hyperthermia has been shown to increase neural injury.169 Therefore, hyperthermia in the postnenral ischemia is avoided with the use of antipyretics and cooling blankets. Clinical trials have not shown any pharmacological therapy to provide neuroprotection after ischemia. The Brain Resuscitation Clinical Trial I did not confirm improved neurological results with barbiturate infusion in patients surviving cardiac arrest. ]72 Calcium channel blockers, lidoflazine. 173 and nimodipine 17+,a75also failed to show benefit in two separate multicenter trials. Corticosteroids 176 and diuretics in the postischemic setting have not been proven beneficial. The mechanism of neurological injury is complicated: therefore the pharmacological approach to limiting neurological damage may be complex as well. SUMMARY

The provision of BLS and ACLS has undergone numerous revisions based on experimental and clinical data. Newer airway devices such as the pharyngotracfieal airway and the C0mbi-tube, are available for alternate airway management. For the cardiac arrest patient, BLS is only a temporizing measure until ACLS can be delivered. The early application of defibrillation yields a higher intermediate and long-term survival in

CURRENT CONCEPTS IN CARDIOPULMONARY RESUSCITATION

403

!

• • • •

Continua CPR Fntubate at once Obtain IV access Confirm asystole in more than one lead

I

I

Consider possible causes • Hypoxia • Hyperkalemia = Hypokalemia • Preexisting acidosis • Drug overdose • Hypothermia

Consider immediate transcutaneous pacing

(TCP)*

• Epinephrine 1 mg IV push, 1-.1: repeat every 3-5 min

• Atropine 1 mg IV, repeat every 3-5 rain up to a total of 0.04 rng/kg§ll

Consider • Termination of efforts¶

Fig 15.

I

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Class I: definitely helpful Cla88 lie acceptable, probably helpflJl Class lib: acceptable, p o ~ helpful Class Ill: not indicated, may be ha/mful *TCP is a Class lib interventJor~. Lack of success may be due to delays in paring. To be effective TCP must be performed •arty, s~naltaneously with drugs. Evidence does not soppu~ roul~ne use of TCP for asystole, 1"The recommended dose of ep/nephr/ne is 1 mg IV push every 3-5 rain. if this approach falls, several Class lib dosing regimens can be considered: • Intermediate: epinep/~ne 2-5 mg IV push, every 3-5 rain • Escala~ng: epinephr/ne 1 mg-3 rag-5 rng IV push (3 rain apart) • HkJh: ep/nephnne 0.1 rng~g IV push, every 3-5 min ~.Sodlurn b/carbccJMe 1 mEq/l~g is Class I if patient has known preexL~ing hyperkalemia.

~Shoder atropine dosing intervals are Class lib in asysto(ic arrest. IlSodium b/carboram 1 mEq~g: ClaSs Ila • if known preex~ng bicarbonate-responsive a~tns~s • if overdose with tdcydic az~depressants into alkalinize the urine in drug overdoses Class lib • if irrrubated and corr,~nued iorlg arrest interval • up(~ return of spontaneous dmulation after long arrest interval Class }11 • hypox¢ isctic a ~ ¶If patient rem~ns in asystole or other agonat rhythms after successful intubati~ and inilJ~ medicatk~s and no reversib#ecauses are ~ , consider terminalk~ of rescac=ta0veefforts by a physeian. Consider interval since arrest

Algorithm for asystole. (From the American Heart Association, 7s with permission.)

pulseless VT or VF. Basic emergency medical technicians or first responders are now using automatic external defibrillators on out-of-hospital cardiac arrest patients. Pharmacological intervention has broadened with the introduction of adenosine. Adenosine has provided both diagnostic and therapeutic applications in both narrow-complex (supraventricular) and widecomplex (supraventricular or ventricular) tachycardia. The indications for calcium and sodium bicarbonate are now limited to more specific applications. Interposed abdominal counterpulsation CPR (IAC CPR) and active compression-decompression CPR (ACD CPR) are techniques that require further investigation before the current A H A CPR guidelines are changed. The use of ahernative-dose epinephrine in cardiac arrest is considered acceptable and

possibly helpful, although no data have shown improved survival to discharge. The recognition and treatment of cardiopulmonary arrest requires the knowledge of airway management and ventilation; circulation and perfusion; defibrillation, cardioversion, and pacing; and pharmacological intervention. Practicing physicians must continue to update themselves on what is proven technology and practice, and what remains investigational to provide appropriate care during a cardiopulmonary resuscitation. ACKNOWLEDGMENT The authors thank Kimberly Sankey for her assistance in the preparation of this manuscript.

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