Open-chest cardiopulmonary resuscitation: past, present and future

Open-chest cardiopulmonary resuscitation: past, present and future

Resuscitation 64 (2005) 149–156 Review Open-chest cardiopulmonary resuscitation: past, present and future夽 Ana G. Alzaga-Fernandeza , Joseph Varonb,...

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Resuscitation 64 (2005) 149–156

Review

Open-chest cardiopulmonary resuscitation: past, present and future夽 Ana G. Alzaga-Fernandeza , Joseph Varonb,∗ b

a Universidad Autonoma de Tamaulipas School of Medicine, Tampico, Mexico The University of Texas Health Science Center, St. Luke’s Episcopal Hospital, 2219, Dorrington St., Houston, TX 77030, USA

Received 23 June 2004; accepted 23 June 2004

Abstract Out-of-hospital cardiac arrests account for approximately 1000 sudden cardiac deaths per day in the United States. Since its introduction in 1960 closed-chest cardiac massage (CCCM) often takes place as an attempt at resuscitation, although its survival rates are low. Other resuscitation techniques are available to physicians such as open-chest cardiopulmonary resuscitation (OCCPR). OCCPR has been shown by several scientists to be hemodynamically superior to CCCM as it increases arterial pressures, cardiac output, coronary perfusion pressures, return of spontaneous circulation and cerebral blood flow. Improved neurological and cardiovascular outcome and an increase in survival rate compared to CCCM have been described. Timing is one of the key variables in determining patient outcome when performing OCCPR. The American Heart Association in association with the International Liaison Committee (ILCOR) has specific indications for the use of OCCPR. Some investigators recommend starting OCCPR in out-of-hospital cardiac arrests on arrival at the scene instead of CCCM. Surprisingly, the incidence of infectious complications after thoracotomy in an unprepared chest is low. The vast majority of the patients’ families accept OCCPR as a therapeutic choice for cardiac arrests and it has been showed to be economically viable. This paper reviews some of the basic and advanced concepts of this evolving technique. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Open-chest cardiopulmonary resuscitation; Closed-chest massage; Invasive techniques; Minimally invasive; Thoracotomy

Contents 1.

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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2.

Historical aspects of OCCPR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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3.

Studies comparing OCCPR to other resuscitation techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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4.

Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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5.

Newer techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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6.

Timing of OCCPR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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7.

Indications for OCCPR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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8.

Acidosis and OCCPR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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夽 A Spanish and Portuguese translated version of the Abstract and Keywords of this article appears at 10.1016/j.resuscitation.2004.06.022. ∗

Corresponding author. Tel.: +1 713 669 1670; fax: +1 713 839 1467. E-mail address: [email protected] (J. Varon).

0300-9572/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2004.06.022

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9.

Epinephrine (adrenaline) and OCCPR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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10.

OCCPR in the pediatric population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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11.

Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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12.

Economic issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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13.

Psychological impact. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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14.

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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1. Introduction Coronary artery disease with arrhythmias remains the most common cause of death in the United States with an estimated incidence of out-of-hospital cardiac arrest of approximately 1000 sudden cardiac deaths per day [1]. Since the widespread introduction of closed-chest cardiac massage (CCCM) into the clinical practice by Kouwenhoven et al. in 1960, resuscitation attempts have been performed in a variety of clinical settings [2]. Despite its widespread use, CCCM has low resuscitation rates. Other techniques of cardiac massage are also available to clinicians. One such technique is open-chest cardiopulmonary resuscitation (OCCPR). For more than 100 years, OCCPR has been shown to be effective in some cases and to be hemodynamically superior to CCCM in many clinical and research scenarios [3–6]. The purpose of this paper is to review historical data that led to the development of the modern types of OCCPR as well as its hemodynamic advantages and clinical data for practitioners who deal with resuscitation situations on regular basis.

2. Historical aspects of OCCPR OCCPR has been recognized as a viable resuscitation technique for over a century [7]. Attempts to examine the heart function are attributed to the Chinese and the Aztecs [8]. However, the fundamental principles of OCCPR are attributed to Moritz Schiff, a distinguished Frankfurt physiologist [7,9,10]. In 1874, Schiff investigated the effects of chloroform and ether on dogs and practiced OCCPR on them after their hearts ceased to beat [11]. These animal physiology studies were followed by Paul Niehans, who was the first to attempt OCCPR on humans in 1880 after Schiff’s description [12]. He described the use of this ‘new’ technique on a 40-year-old man who had a cardiac arrest prior to undergoing general surgery. Unfortunately, this attempt at resuscitation using OCCPR was unsuccessful. Years later, in 1898, Tuffier and Hallion performed OCCPR in a patient with a suspected pulmonary embolism [13]. Despite obtaining return of spontaneous circulation (ROSC),

the patient had a second cardiac arrest and died soon thereafter. Prus, at the turn of the century, published the results of resuscitation by direct cardiac compressions in dogs that had undergone asphyxia, chloroform inhalation, and electrical shocks [14]. Kristian Ingelsrud, in 1901, was the first physician to achieve a successful outcome after OCCPR as an emergency treatment for cardiac arrest [15]. The patient was a previously healthy lady who developed a cardiac arrest during an elective hysterectomy. A year later, Lane and Gray performed a subdiaphragmatic approach to cardiac massage and successfully resuscitated a patient [16]. Less than 5 years later, in 1906, Greene reported 40 cases of successful resuscitation using OCCPR with a 22% complete recovery rate [17]. Clearly, the development of newer anesthesia techniques to facilitate thoracic surgery in the early 1930s contributed to the more frequent practice of OCCPR [18]. Several decades later, Lee and Downs reported an overall survival rate of 25%, which made OCCPR the method of choice until 1960 [19]. Stephenson et al. published in 1953 a report of 1200 cardiac arrest victims with a 28% survival rate with OCCPR [20]. When Kouwenhoven, Jude and Knickerbocker described CCCM in detail in 1960 with an associated 70% long-term survival rate, the use of OCCPR declined [21,22].

3. Studies comparing OCCPR to other resuscitation techniques The rediscovery of CCCM by Kouwenhoven and coworkers stimulated the experimental comparison between external and internal cardiopulmonary resuscitative techniques [23]. A variety of physiological variables were initially compared and included: pulse palpation; arterial, venous, intrathoracic and intracranial pressures; acid–base and oxygenation variables; ROSC and return of spontaneous respiratory efforts; neurological status and survival rates, among others [24–28] (see Table 1). In a canine cardiac arrest model, Redding and Cozine showed results using both types of resuscitation after electrically induced ventricular fibrillation (VF) [29]. The com-

A.G. Alzaga-Fernandez, J. Varon / Resuscitation 64 (2005) 149–156 Table 1 Physiological differences between OCCPR and CCCM

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Table 2 Changes in arterial and perfusion pressures according to technique

OCCPR

Variables

CCCM

↑↑ ↓ =/↓ ↑↑ ↑↑ ↑ ↑↑

Arterial pressures Venous pressures Intrathoracic pressure Cardiac output/cardiac index Return of spontaneous circulation Neurological status Survival rates

↑ ↑ ↑ ↑ ↑ ↓ ↑/↓

mon carotid artery blood flow (CCABP), arterial pressures, and cardiac resuscitability revealed no significant differences between the methods. Weale and Rothwell-Jackson in another canine model found higher arterial and mean perfusion pressures and lower venous pressures when switching from CCCM to OCCPR [30]. Weiser et al. found that OCCPR could increase the cardiac output (CO) by 300% and double mean arterial blood pressure (MAP) in two subsets of cardiac arrests induced in dogs (normal and with myocardial infarction) [31]. In experimental animal model, Bircher and Safar demonstrated that OCCPR improved carotid blood flow, systemic arterial pressure, and coronary artery perfusion pressure [32]. In another experimental study by Rubertsson et al., improved systemic perfusion was achieved with OCCPR, especially during the cardiac relaxation phase [33]. In a similar experimental study, Boczar et al. found a significant difference between the coronary perfusion pressure (CPP) gained with CCCM and OCCPR [34]. In this study, OCCPR had CPP levels that exceeded those associated with ROSC by 15 mmHg. In a well-controlled study, Del Guercio et al. demonstrated that OCCPR in humans doubled the cardiac index (CI), but did not raise the MAP significantly [35]. In another human study, Geehr found that the 24 h survival rate was significantly higher with OCCPR than with CCCM [36]. Whether or not these perfusion pressures are related to the duration of OCCPR is a matter of controversy. Halperin et al. demonstrated that CPP was not dependant on the duration of the compression but rather on the rate of compression [37]. In this study, it was interesting to note that the stroke volume was related to the change in the ventricular shape. From a cerebral perfusion standpoint, Byrne et al. were the first to measure cerebral blood flow (CBF) during CPR in a systematic manner using microspheres [38]. In their study, they could maintain a near-normal CBF in the cerebral cortex and cerebellum during OCCPR in dogs after 1 min of the arrest compared to only 30% of the CBF obtained with CCCM. Yashon et al. demonstrated the ability of OCCPR to restore and maintain relatively normal electroencephalographic (EEG) activity for up to 1 h after a 4-min period of cardiac arrest [39]. Gamelli et al. showed close-to-normal CBF variables and postulated possible cerebral metabolic benefits of OCCPR on cerebral tissue [40]. In contrast, Luce et al. demonstrated in an animal model that CCCM only provides CBF in the range of 15–30% of precardiac arrest values

OCCPR CCCM

↑↑ Coronary perfusion pressure ↑↑ Cerebral perfusion pressure ↑ Right arterial pressure peaks

↑ Blood flows

[41]. White et al. showed in a canine preparation, improved brain mitochondrial preservation with OCCPR according to the content of mitochondrial superoxide dismutase which is associated with a normal neurological outcome [42]. In their classic paper, Bircher and Safar showed an improved neurological and cardiovascular outcome in dogs after 30 min of OCCPR compared with CCCM [32]. In this study, OCCPR doubled flow and enhanced aortic compression with the direction of perfusion to the brain and coronary arteries. Dr. Peter Safar concluded from his seminal studies that: “The main reason why the open-chest method is physiologically superior is the fact that sternal compressions cause right atrial pressure peaks as high as arterial cerebral perfusion pressures. Direct massage of the ventricles does not increase right atrial pressure and produces high, controllable coronary and cerebral perfusion pressures and blood flows” [43] (see Table 2).

4. Techniques There are several different techniques for performing an emergency thoracotomy for resuscitative purposes (see Fig. 1). Perhaps the most common is the left anterolateral thoracotomy approach [44]. In this surgical technique, an incision is performed over the left fifth rib from the sternum to mid-axillary line [45]. This is followed by blunt digital dissection of the fourth intercostal space muscles followed by the introduction of a rib spreader or similar instrument. Once the pericardium is encountered, it is opened and manual compressions begun. For penetrating injuries of the inlet,

Fig. 1. Different approaches to OCCPR: (1) left anterolateral thoracotomy; (2) midline sternotomy; (3) MID-CM.

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ventricle, or use the fingers of the right hand compressing the heart against the sternum. These two techniques were noted to perform better than holding the heart with one hand alone. The rate at which the heart is manually compressed varies between 60 and 100 min−1 . Some authors suggest 80–100 min−1 , while others recommend a compression rate of 60 min−1 , since an increase in the rate is followed by marked digital exhaustion and is unrealistic for clinical practice [24,49].

5. Newer techniques Fig. 2. Left lateral thoracotomy.

the left thoracotomy at this level is an appropriate approach [44] (see Fig. 2). Midline sternotomy is another technique commonly used in cardiac and lung surgery. It has been used in cardiac arrest during these operations as well. It is also employed for stab wounds in the precordial region in patients with cardiac tamponade. This approach provides a good exposure of the heart, superior anterior mediastinum and hilum of the lung [44]. More recently, a minimally invasive approach has been developed and introduced by Buckman et al. [46,47]. This innovative procedure is performed by making a small incision at the fourth intercostal space, 5 cm left from the sternal midline. In this technique, it is suggested that exploration of the pericardial surface is performed with a gloved index finger after the incision, to detect pericardial adhesions and abort the procedure, if any are found. Using a telescopic instrument with a deployment mechanism, cardiac compressions are done gently with a 4-cm stroke in an anterior posterior direction perpendicular to the chest wall plane (see Fig. 3). There is significant controversy as to the “best” techniques when performing OCCPR [48,49]. Barnett et al., in a canine cardiac arrest model, compared various OCCPR techniques after exposing the heart through a lateral thoracotomy [49]. These authors concluded that the most effective techniques were either to use both hands with the left hand holding the right ventricle and the fingers of the right hand holding the left

Fig. 3. MID-CM technique.

Minimally invasive direct cardiac massage (MID-CM) is an atraumatic manual cardiac pumping system deployed through a small incision in the thorax [50]. Buckman et al. demonstrated that direct cardiac massage can be given through a limited, parasternal, intercostal incision into which the device can be inserted [46,47] (see Fig. 3). Manual compression of the device produces an artificial systole through a minimally invasive approach. The benefits of a minimally invasive approach are that it can be performed quickly, with limited surgical skills and equipment [46,47]. Paiva et al. showed that MID-CM was superior to CCCM for ROSC and CPP at 30 min of CPR [51]. There were no significant injuries that altered the outcome when this technique was being used. With the proper and placed placement of the device, this technique has proven to be a helpful adjunct to advanced life support [51].

6. Timing of OCCPR As in any case of cardiac arrest, the interval between arrest and the institution of advanced cardiac life support techniques is of extreme importance [52]. There have been anecdotal cases of survival after 2.5 h of OCCPR [53]. Shocket and Rosenblum described successful resuscitation with OCCPR in one patient after 75 min of CCCM [54]. Many studies have attempted to determine the best time for the institution of OCCPR. Sanders and co-workers in a cardiac arrest canine model showed that 75% of the study animals were resuscitated when OCCPR was started within 15 min of cardiac arrest [55]. It is interesting to note that this percentage dropped to 40% when the thoracotomy was delayed to 20 min. Kern and co-workers, in another canine experiment, determined that after 20 min of untreated ventricular fibrillation, OCCPR could achieve initial recovery but did not produce long-term survival [56]. In a human study, Geehr demonstrated similar findings when OCCPR was instituted after arrival at the emergency department, usually after 30 min or more from the time of initial cardiac arrest [36]. In out-of-hospital cardiac arrest situations, Takino and Okada suggest that the thoracotomy should be done within 5 min of hospital arrival in order to obtain the highest rate of ROSC [57]. This rate declines as the timing of the interven-

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tion is delayed. These results suggest that if the thoracotomy is done early during this initial period, the incidence of futile thoracotomies will be maintained at a minimum. For patients who have undergone cardiac surgery, emergency thoracotomy and OCCPR should be considered as an early intervention during cardiac arrest [58]. In hemodynamically stable patients, successful resuscitation depends on the prompt correction of mechanical factors that lead to sudden cardiac arrest as well the timing of the thoracotomy [59]. The patients most likely to benefit were those within 24 h of surgery, and in whom chest reopening was achieved within 10 min of the time of arrest [60]. It is important to recognize that there is a window of opportunity that should be targeted to start OCCPR in order to obtain the best outcome results [61]. Time is the single most important variable in the treatment of cardiac arrest [62]. Successful resuscitation cannot be expected when instituting OCCPR after a prolonged period of ineffective CCCM [56]. The timing of switching from CCCM to OCCPR will determine the outcome and prognosis of a patient in cardiac arrest [57].

7. Indications for OCCPR According to the Guidelines 2000 from the American Heart Association in association with ILCOR, an emergency thoracotomy is indicated in patients who develop cardiac arrest with penetrating chest trauma, hypothermia, pulmonary embolism, hyperinflation of the lungs, pericardial tamponade, chest deformity and penetrating abdominal trauma [63]. Other recommendations for OCCPR include medical cardiac arrests in which external chest compressions with advanced life support fail to restore spontaneous circulation within 5–10 min [64] (see Table 3). Paradis et al. published three cases with a positive outcome in which OCCPR was performed after the failure of CCCM [62]. These patients had suffered cardiac arrest due to different causes: intravenous drug abuse, coronary artery disease and high-voltage electric shock, and all of them made a successful recovery. Hachimi-Idrissi et al. have tried switching to OCCPR outof-hospital when attempts at CCCPR have failed and proved it to be feasible and accepted by the public [65]. Over a period of Table 3 Possible indications for OCCPR Indications Penetrating chest trauma Pulmonary embolism Pericardial tamponade Penetrating abdominal trauma Chest deformity Hyperinflation of the lungs Hypothermia Out-of-hospital cardiac arrests

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12 years, these investigators performed OCCPR in 33 patients with out-of-hospital cardiac arrest, when CCCM efforts to achieve ROSC had been unsuccessful. Although OCCPR was more effective in obtaining ROSC, the survival rate was low due to the overall period of cardiac arrest followed by the period of low output produced by CCCM. These investigators recommend starting OCCPR immediately on arrival at scene instead of CCCM.

8. Acidosis and OCCPR During cardiac arrest, tissue perfusion decreases and fails to maintain adequate oxygen delivery [67]. This, in turn, causes anaerobic metabolism and accumulation of CO2 and lactate in peripheral tissues, from which it is gradually released into the circulating blood [66]. Henneman et al. studied a sample of 16 patients undergoing 5 min of CCCM followed by 5 min of OCCPR. The development of acidosis, as measured by arterial blood gases, was not significantly different for both subgroups [67]. In animal models, lactic acidosis increases with CCCM and stabilizes with OCCPR [62,68,69]. It is unclear if the stabilization is due to decreased lactate production (improved tissue perfusion), improved extraction and metabolism of lactate by the liver, or delayed or impaired release of lactate from poorly perfused peripheral tissue [67]. The treatment of metabolic acidosis during CPR with bicarbonate is controversial. Data suggest that buffer administration not only lacks benefits, but also may be deleterious in the treatment of lactic acidosis [70]. Studies have demonstrated that after effective intracellular buffering, glycolysis can continue to produce lactate for a longer period than when a buffer with an intracellular effect is not used [67]. The effect of a buffer is also short-lasting, and that more would have been needed at a later stage of the experiment if a higher or more normal pH had been the aim [71]. Therefore, the fundamental principle for avoiding further acidosis in a cardiac arrest victim is to restore the systemic circulation rather than focusing on buffer therapy.

9. Epinephrine (adrenaline) and OCCPR The use of epinephrine and norepinephrine (noradrenaline) has been studied to determine the enhancement of OCCPR during cardiac arrest. Early administration of epinephrine enhances resuscitability during experimental CPR by increasing blood pressure and therefore increasing coronary artery blood flow [72,73]. Several authors have found increased blood flow in the brain and myocardium after epinephrine administration [74]. Nevertheless, epinephrine lowers the pulmonary artery flow, probably as a result of increased total peripheral vascular resistance. Its constrictive effect is greater on peripheral vessels than on vessels that supply the brain or the heart [75]. In an animal study, Rubertsson

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and Wiklund demonstrated that the effect of epinephrine during CPR is short-lasting, and declined after only 2 min. The systemic blood pressure and the blood flow in the pulmonary artery returned toward the pre-epinephrine values [71]. Lindner et al., in another canine study, showed that epinephrine and norepinephrine increase the cerebral perfusion pressure, and do not increase the cerebral oxygen consumption or decrease the cerebral oxygen extraction [77]. 10. OCCPR in the pediatric population A pediatric canine model developed by Fleisher et al. demonstrated that OCCPR produced a greater cardiac output and a higher cerebral blood flow compared to CCCM [76]. The rate of recovery from arrest was greater, and the incidence of complications was smaller, among those receiving OCCPR. Just as in the adult population, the duration of cardiac arrest in children is critical for a successful resuscitation [76]. After a period of 20 min, OCCPR may not offer long-term benefits [78]. The efficacy of the resuscitation relies in early use of OCCPR in children after cardiac arrest [78]. In a study by Toshihisa and co-workers, questionnaires were handed out to the families of victims of cardiac arrest to ascertain their opinion of OCCPR as a resuscitative technique in children. From the 238 families in the study, only 14 (5.8%) did not agree with the use of this procedure in pediatric patients [79]. This low rejection percentage compares to the lower acceptance this technique has in elderly patients, in which it was denied by 52 families (21.8%). As a result, OCCPR seems to be a realistic option in the emergency treatment of pediatric arrest. 11. Complications Infectious complications should not be a concern as the rate of empyema secondary to thoracotomy in the unprepared chest is less than 10% [80,81]. Moreover, Altemeier and Todd found a surprisingly low incidence of infection (5%), none of them having a fatal outcome when emergency thoracotomy is performed in non-sterile conditions [82]. Bircher and coworkers have published data indicating the incidence of thoracic wound infection ranging from 0.0 to 9.1% [83]. CCCM has several potential complications, many which are undetected. During CCCPR, organs can be damaged and this may not be noticed immediately. There have been reports of broken ribs, liver lacerations and heart injuries, such as left or right ventricle rupture [84]. The incidence of iatrogenic damage in OCCPR is 0.0–1.4% [83].

12. Economic issues It has been said that OCCPR is ‘too expensive’ to be part of the routine resuscitation protocol [3]. The costs for OCCPR

are higher only for those patients for whom it is successful. The price of the basic necessary equipment is small compared with the overall cost of the resuscitation team.

13. Psychological impact Toshihisa and co-workers showed that the younger generation generally accepted OCCPR as a therapeutic choice for cardiac arrest [79]. It was interesting to learn that most families unconditionally consented to aggressive OCCPR, when they became calm after the sudden event of cardiac arrest of their family member. Nevertheless, it is essential to explain the situation and condition to the patient’s family carefully after OCCPR.

14. Conclusions The object effective CPR is to restore the spontaneous systemic circulation as soon as possible to avoid any neurological damage and to obtain higher survival and outcome rates. Experimentally, OCCPR increases the time window for successful resuscitation and has demonstrated to be superior in maintaining hemodynamic variables almost in the normal physiological range. Hence, OCCPR should be integrated with CCCPR into a logical resuscitation protocol which will assure better survival opportunities.

References [1] Becker LB, Smith DW, Rodees KV. Incidence of cardiac arrest: a neglected factor in evaluating survival rates. Ann Emerg Med 1993;22:86–91. [2] Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed chest cardiac massage. J Am Med Assoc 1960;173:1064–7. [3] Del Guercio LRM. Open chest cardiac massage: an overview. Resuscitation 1987;15:9–11. [4] Alifimoff JK. Open versus closed chest cardiac massage in nontraumatic cardiac arrest. Resuscitation 1987;15:13–21. [5] Rosenthal RE. Cardiopulmonary resuscitation: historical and future perspectives. Postgrad Med 1987;81, 90–2, 101–3. [6] Eldor J, Frankel DZN, Davidson JT. Open chest cardiac massage: a review. Resuscitation 1988;16:155–62. [7] Vallejo-Manzur F, Varon J, Fromm R, Baskett P. Moritz Schiff and the history of open-chest cardiac massage. Resuscitation 2002;53:3–5. [8] Lyons AS, Petrucelli J. Medicine: An Illustrated History. New York: H N Abrams; 1978. pp. 127, 159, 432–7. [9] Pike FH, Guthrie CC, Steward GN. Studies in resuscitation. I. The general condition affecting resuscitation and the resuscitation of the blood and the heart. J Exp Med 1908;10:371–418. [10] Jude JR. Personal reminiscences of the origin and history of cardiopulmonary resuscitation. Am J Cardiol 2003;92:956–63. [11] Hake TG. Studies on ether and chloroform from Prof. Schiff’s physiology laboratory. Practitioner 1847;12:241–50. [12] Zesas DG. Zur frage der Hermassage beim Chloroformkollaps. Cantralblatt fur Chirugie 1903;17:588–9.

A.G. Alzaga-Fernandez, J. Varon / Resuscitation 64 (2005) 149–156 [13] Tuffier T, Hallion M. De la compression rhythmic du Coeur dans la syncope cardiaque par embolic. Bull Membr Soc Chir 1898;24:937–9. [14] Prus J. Ubre die Wiederbelebung in Todesfallen in Folge von Erstickung Chloroformvergiftung und elektrischem Schlage. Wien klin Wochenscr 1900;13:451–8. [15] Keen WW. Case of total laryngectomy (unsuccessful) and a case of abdomen hysterectomy (successful) in both which massage of the heart for chloroform collapse was employed, with notes of 25 other cases of cardiac massage. Ther Gaz 1904;28:217–20. [16] Pearson JW. Historical and Experimental Approaches to Modern Resuscitation. Springfield, IL: Charles C Thomas; 1965, 1–93. [17] Greene DG. General considerations. In: Whittenberger JL, editor. Artificial Respiration: Theory and Application. New York: Hoeber; 1962. p. 35–68. [18] Hermreck AS. The history of cardiopulmonary resuscitation. Am J Surg 1998;156:430–6. [19] Lee WE, Downs TM. Resuscitation by direct massage of the heart in the cardiac arrest. Ann Surg 1924;80:555–61. [20] Stephenson HE, Reid LC, Hinton JW, et al. Some common denominators in 1200 cases of cardiac arrest. Ann Surg 1953;137: 731–44. [21] Gazmuri RJ, Becker J. Cardiac resuscitation: the search for hemodynamically more effective methods. Chest 1997;111:712–23. [22] Thangam S, Weil MH, Rackow EC. Cardiopulmonary resuscitation: a historical review. Acute Care 1986;12:63–94. [23] Bircher N, Safar P. Open-chest cardiopulmonary resuscitation: an old method whose time has returned. Am J Emerg Med 1984;6: 568–71. [24] Calinas-Carreia J, Phair I. Physiological variables during open-chest cardiopulmonary resuscitation: results form a small series. J Accid Emerg Med 2000;17:201–4. [25] Jackson RE, Freeman SB. Hemodynamics of cardiac massage. Emerg Med Clin North Am 1983;1:501–13. [26] Kern KB, Sanders AB, Badylak SF, et al. Long-term survival with open-chest cardiac massage after ineffective closed-chest compression in a canine preparation. Circulation 1987;75:498–503. [27] Martin GB, Carden DL, Nowak RM, Tomlanovich MC. Central venous and mixed venous oxygen saturation: comparison during canine open-chest cardiopulmonary resuscitation. Am J Emerg Med 1985;3:495–7. [28] Martin GB, Carden DL, Nowak RM, Tomlanovich MC. Comparison if central venous and arterial pH and pCO2 during open-chest cardiopulmonary resuscitation in the canine model. Ann Emerg Med 1985;14:529–33. [29] Redding JS, Cozine RA. A comparison of open-chest and closedchest cardiac massage in dogs. Anesthesiology 1961;22:280–5. [30] Weale FE, Rothwell-Jackson RL. The efficiency of cardiac massage. Lancet 1962;1:990–2. [31] Weiser FM, Adler LN, Kunn LA. Hemodynamic efforts of closed and open-chest resuscitation in normal and those with acute myocardial infarction. Am J Cardiol 1962;10:555–61. [32] Bircher N, Safar P. Comparison of standard “new” closed-chest cardiopulmonary resuscitation and open-chest cardiopulmonary resuscitation in dogs. Crit Care Med 1981;9:384–5. [33] Rubertsson S, Grenvik A, Wiklund L. Blood flow and perfusion pressure during open-chest versus closed-chest cardiopulmonary resuscitation in pigs. Crit Care Med 1995;23:715–25. [34] Boczar ME, Howard MA, Rivers EP, et al. A technique revisited: hemodynamic comparison of closed and open-chest cardiac massage during human cardiopulmonary resuscitation. Crit Care Med 1995;23:498–503. [35] Del Guercio LRM, Feins NR, Cohn JD, Coomaraswamy RP, Wollman SD, State D. Comparison of blood flow during external and internal cardiac massage in man. Circulation 1965;31:171–80. [36] Geehr EC. Open-chest cardiac massage for victims of medical cardiac arrest. Ann Emerg Med 1985;14:498.

155

[37] Halperin HR, Tsitlik JE, Guerci AD, et al. Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs. Circulation 1986;73:539–50. [38] Byrne D, Pass HI, Neely WA, et al. External versus internal cardiac massage in normal and chronically ischemic dogs. Ann Surg 1980;46:657–62. [39] Yashon FC, Wagner FC, Massopust LC, et al. Electrocorticographic limits of cerebral viability during cardiac arrest and resuscitation. Am J Surg 1971;121:728–31. [40] Gamelli R, Saucier J, Browdie D. An analysis of cerebral blood flow systemic base deficit accumulation and mean arterial pressure as a function of internal cardiac massage rates. Am J Surg 1979;45:26–33. [41] Luce JM, Rizk GB, Rivers EP. Use of open chest cardiopulmonary resuscitation after failure of standard closed chest cardiopulmonary resuscitation: illustrative cases. Resuscitation 1992;24:61–71. [42] White BC, Hildebrant JF, Evans AT. Prolonged cardiac arrest and resuscitation in dogs: brain mitochondrial function with different artificial perfusion methods. Ann Emerg Med 1985;14:383–8. [43] Tisherman SA, Vandevelde K, Safar P, et al. Future directions for resuscitation research V. Ultra-advanced life support. Resuscitation 1997;34:281–93. [44] Ivatury RR, Rohman M. Emergency department thoracotomy for trauma: a collective review. Resuscitation 1987;15:23–35. [45] Del Guercio LR. A plea for open-chest cardiopulmonary resuscitation. Am J Emerg Med 1984;2:565–6. [46] Buckman RF, Badellino MM, Mauro LH, et al. Direct cardiac massage without major thoracotomy: feasibility and systemic blood flow. Resuscitation 1995;29:237–48. [47] Buckman RF, Badellino MM, Eynon CA, et al. Open-chest cardiac massage without major thoracotomy: metabolic indicators of coronary and cerebral perfusion. Resuscitation 1995;34:247–53. [48] Babbs CF. Hemodynamic mechanisms in CPR: a theoretical rationale for resuscitative thoracotomy in non-traumatic cardiac arrests. Resuscitation 1987;15:37–50. [49] Barnett WM, Alifimoff JK, Paris PM, et al. Comparison of open-chest cardiac massage techniques in dogs. Ann Emerg Med 1986;15:408–12. [50] Rozenberg A, Incagnolia P, Delpecha P, et al. Prehospital use if minimally invasive direct cardiac massage (MID-CM): a pilot study. Resuscitation 2001;50:257–62. [51] Paiva EF, Kern KB, Hilwig RH, et al. Minimally invasive direct cardiac massage versus cardiopulmonary resuscitation in a porcine model of prolonged ventricular fibrillation cardiac arrest. Resuscitation 2000;47:287–99. [52] Kern KB, Sanders AB, Janas W, et al. Limitations of open-chest cardiac massage after prolonged untreated cardiac arrest in dogs. Ann Emerg Med 1991;20:761–7. [53] Russell ES. Cardiac arrest: survival after 2.5 h open-chest cardiac massage and survival after closed-chest cardiac massage. Can Med Assoc J 1962;87:512–3. [54] Shocket E, Rosenblum R. Successful open-chest massage after 75 min of closed-chest massage. Ann Emerg Med 1984;2:138–40. [55] Sanders AB, Kern KB, Ewet GA. Time limitations for open-chest cardiopulmonary resuscitation from cardiac arrest. Crit Care Med 1985;13:897–8. [56] Kern KB, Sanders AR, Ewy GA. Open-chest cardiac massage after closed-chest compression in a canine mode: when to intervene. Resuscitation 1987;15:51–7. [57] Takino M, Okada Y. The optimum timing of resuscitative thoracotomy for non-traumatic out-of-hospital cardiac arrest. Resuscitation 1993;26:69–74. [58] Pottle A, Bullock I, Thomas J, Scott L. Survival to discharge following open chest cardiac compression: a 4-year retrospective audit in a cardiothoracic specialist centre – Royal Brompton and Harefield NHS Trust, United Kingdom. Resuscitation 2002;52: 269–72.

156

A.G. Alzaga-Fernandez, J. Varon / Resuscitation 64 (2005) 149–156

[59] Anthi A, Tzelepis GE, Alivizatos P, Michalis A, Palatianos GM, Geroulanos S. Unexpected cardiac arrest after cardiac surgery: incidence, predisposing causes, and outcome of open-chest cardiopulmonary resuscitation. Chest 1998;113:15–9. [60] Mackay JH, Powell SJ, Osgathorp J, Rozario CJ. Six-year prospective audit of chest reopening after cardiac arrest. Eur J Cardiothorac Surg 2002;22:421–5. [61] Sanders AB. Open-chest CPR, not yet. Am J Emerg Med 1984;2:566–7. [62] Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. J Am Med Assoc 1990;263:1106–13. [63] American Heart Association. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6. Advanced cardiovascular life support. Circulation 2000:107–11. [64] Safar P. On the future of reanimatology. Acad Emerg Med 2000;7:75–89. [65] Hachimi-Idrissi S, Leeman J, Hubluoe Y, et al. Open chest cardiopulmonary resuscitation in out-of-hospital arrest. Resuscitation 1997;35:151–6. [66] Fillmore SJ, Shapiro M, Killip T. Serial blood gas studies during cardiopulmonary resuscitation. Ann Intern Med 1970;72: 465–9. [67] Henneman PL, Gruber JE, Marx JA. Development of acidosis in human beings during closed-chest and open-chest cardiopulmonary resuscitation. Ann Emerg Med 1988;17:672–5. [68] Carden DL, Martin GB, Nowak RM, et al. Lactic acidosis as a predictor of downtime during cardiopulmonary arrest in dogs. Am J Emerg Med 1985;3:120–4. [69] Carden DL, Martin GB, Nowak RM, et al. Lactic acidosis during closed-chest cardiopulmonary resuscitation in dogs. Ann Emerg Med 1985;14:496. [70] Graf H, Leach W, Arrieff AI. Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science 1985;227:754–6. [71] Rubertsson S, Wiklund L. Hemodynamic effects of epinephrine in combination with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation. Crit Care Med 1993;21:1051–7.

[72] American Heart Association. Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). J Am Med Assoc 1986;255:2841–3044. [73] Paradis NA, Martin GB, Rosenberg J, et al. The effect of standardand high-dose epinephrine on coronary perfusion pressure during prolonged cardiopulmonary resuscitation. J Am Med Assoc 1991;265:1139–44. [74] Michael JR, Guerci AD, Koehler RC, et al. Mechanism by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. Circulation 1984;69:822–35. [75] Holmes HR, Babbs CF, Voorhees WD, et al. Influence of adrenergic drugs upon vital organ perfusion during cardiopulmonary resuscitation. Crit Care Med 1980;8:137–40. [76] Fleisher G, Sagy M, Swedlow DB, Belani K. Open- versus closedchest cardiac compressions in a canine model of pediatric cardiopulmonary resuscitation. Am J Emerg Med 1985;3:305–10. [77] Lindner KH, Ahnefeld FW, Pfenninger EG, Schuermann W, Bowdler IM. Effects of epinephrine and norepinephrine on cerebral oxygen delivery and consumption during open-chest cardiopulmonary resuscitation. Ann Emerg Med 1990;19:249–524. [78] Sheik A, Brogan T. Outcome and cost of open- and closed-chest cardiopulmonary resuscitation in pediatric cardiac arrests. Pediatrics 1994;93:392–8. [79] Sakamoto T, Saitoh D, Kaneko N, et al. Is emergency open chest cardiopulmonary resuscitation accepted by patients’ families? Resuscitation 2000;47:281–6. [80] Varon J, Marik PE, Fromm RE. Cardiopulmonary resuscitation: a review for clinicians. Resuscitation 1998;36:133–45. [81] Adelson L. A clinicopathologic study of the anatomic changes in the heart resulting from cardiac massage. Surg Gyn Obstet 1957;104:513–23. [82] Altemeier WA, Todd J. Studies on the incidence of infection following open chest cardiac massage for cardiac arrest. Ann Surg 1963;158:596–607. [83] Bircher N, Safar P. Manual open-chest cardiopulmonary resuscitation. Ann Emerg Med 1984;13:770–2. [84] Kempen PM, Allgood R. Right ventricular rupture during closedchest cardiopulmonary resuscitation after pneumonectomy with pericardiotomy: a case report. Crit Care Med 1999;27:1378–9.