Small animal cardiopulmonary resuscitation requires a continuum of care: proposal for a chain of survival for veterinary patients

Manuel Boller Department of Clinical Studies–Philadelphia, School of Veterinary Medicine (Boller M, Boller E, Otto), and the Department of Emergency Medicine, School of Medicine, University of Pennsylvania (Boller M), Philadelphia, PA 19104; Faculty Division, Ulleval University Hospital, University of Oslo, Oslo, Norway (Oodegard).

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Elise M. Boller Department of Clinical Studies–Philadelphia, School of Veterinary Medicine (Boller M, Boller E, Otto), and the Department of Emergency Medicine, School of Medicine, University of Pennsylvania (Boller M), Philadelphia, PA 19104; Faculty Division, Ulleval University Hospital, University of Oslo, Oslo, Norway (Oodegard).

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Silje Oodegard Department of Clinical Studies–Philadelphia, School of Veterinary Medicine (Boller M, Boller E, Otto), and the Department of Emergency Medicine, School of Medicine, University of Pennsylvania (Boller M), Philadelphia, PA 19104; Faculty Division, Ulleval University Hospital, University of Oslo, Oslo, Norway (Oodegard).

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Cynthia M. Otto Department of Clinical Studies–Philadelphia, School of Veterinary Medicine (Boller M, Boller E, Otto), and the Department of Emergency Medicine, School of Medicine, University of Pennsylvania (Boller M), Philadelphia, PA 19104; Faculty Division, Ulleval University Hospital, University of Oslo, Oslo, Norway (Oodegard).

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Considerable efforts have been made to advance methods of CPR since its introduction 50 years ago. 1,2 As the understanding of CPR has evolved, so has the definition of its major components that contribute to survival. Twenty years ago, the AHA introduced the so-called chain of survival, which serves as a metaphor for the importance of approaching CPA in a timely, sequential, and comprehensive manner. As originally described, the components, or links, in this chain of survival included early access to help, early initiation of CPR, early defibrillation, and early advanced cardiac life support. 3 A number of recent developments in CPR research have encouraged the focused optimization of individual links in the chain of survival, with the goal of optimizing the overall CPR process. 4–7

The AHA published new guidelines for CPR in humans in October 2010. These guidelines, which are revised every 5 years, are based on an evidence evaluation process that serves as the foundation for consensus treatment recommendations. In essence, the AHA aims to identify elements that could further optimize each link of the chain of survival. The first major opportunity for improvement lies in the fact that laypersons and health professionals often do not perform CPR according to published guidelines and that this noncompliance is associated with reduced survival. 6,8–14 Focused efforts are being made to allocate resources that will improve compliance with these guidelines through novel educational and technical tools, and the AHA 2010 CPR guidelines include a new section dedicated to education and implementation. 7,15 Additionally recent studies 16–18 have found clear evidence of the neuroprotective effects of mild therapeutic hypothermia for human patients after CPA, even if administered hours after ROSC. This and the fact that 60% to 70% of humans that have CPA and achieve ROSC subsequently die of post–cardiac arrest syndrome led to the inclusion of a dedicated section on post–cardiac arrest care in the newest AHA CPR guidelines. 19,20 Consequently, postresuscitation care has been suggested as an additional new link in the CPR chain of survival. 21 Similarly, post–cardiac arrest care has been added as one of the key focus points of the recently developed Reassessment Campaign on Veterinary Resuscitation (RECOVER) initiative that for the first time provides consensus-based guidelines for CPR of veterinary patients. 22

The purpose of the present report is to propose a chain of survival for small animals (Figure 1) that reflects the disparities in CPR between human patients and veterinary patients and emphasizes the critical importance of following a coherent strategy for successful treatment of CPA patients. This article highlights select components of each proposed link in the chain.

Figure 1—
Figure 1—

Schematic illustration of the chain of survival for small animals symbolizing the continuum of care required to successfully manage CPA.

Citation: Journal of the American Veterinary Medical Association 240, 5; 10.2460/javma.240.5.540

CPA in Humans and Nonhuman Animals

Each year in the United States alone, an estimated 300,000 people have an OHCA. 23–25 Most of these individuals have clinical or occult coronary artery disease, 24 and approximately 5% to 8% survive to be discharged from the hospital, although this proportion varies from 3% to 16% among different regions of the country 23,26–28 In contrast, CPA in most veterinary patients treated with CPR in large practices and academic centers is related to progressive systemic illness, trauma, or incidents or procedures (eg, anesthesia) that take place in a hospital. 29–31 Although patients with OHCA may be frequently encountered by veterinary practitioners, minimal to no information is presently available in regard to characteristics of this population, whether and how such animals are treated, and subsequent survival rates. In fact, clinical cases reported in veterinary CPR studies 29,31,32 predominantly involve IHCA, and clinical veterinary CPR guidelines 33,34 specifically focus on in-hospital scenarios with several rescuers present. The environmental context of IHCA allows a more expedited and intense care than is typically available for patients with OHCA. However, outcomes after IHCA, although better than those reported after OHCA, are disappointing in humans and poor in companion animals. In humans, survival-to-discharge rates after IHCA vary with arrest rhythm and between pediatric (22.3% to 33.5%) and adult patients (10.0% to 36%). 35,36 Moreover, comorbidities present before CPA (eg, hypotension, sepsis, pneumonia, cancer, and renal failure), advanced age, and number of drugs prescribed were found to be associated with reduced survival rates. 37–42 Survival to discharge after a CPA is uncommon in veterinary medicine, and reported proportions of survivors range from 3% to 6% in dogs and from 2% to 10% in cats. 29,31,32

The First Link: Early Recognition and Prevention

This first link in the chain of survival incorporates 3 distinct concepts as follows: early recognition of patients at risk for CPA, intervention to reduce this risk and thus potentially prevent CPA, and early recognition of CPA once it has developed. An effective strategy should begin with identification of patients at risk during their hospital stay. In the authors' opinions, this could be implemented by having cage-side rounds at shift changes that include all care providers for a given hospital ward. This can facilitate recognition of patients at risk for CPA, and a monitoring protocol can be designed to immediately identify any worsening of the patient's condition. Identified abnormalities can then be corrected in a timely manner, and planned procedures (especially those involving sedation or anesthesia) can be adjusted or delayed as appropriate. A set of mnemonic devices described as the 5 H's and 5 T's can be used as a tool to identify patients at risk for CPA or to assess specific reversible etiologies during CPR. 20 The 5 H's are hypovolemia or hemorrhage, hypoxia or hypoventilation, hydrogen ions (acidosis), hyperkalemia or hypokalemia, and hypoglycemia. The 5 T's include toxins, tension pneumothorax, thromboembolism or thrombosis, tamponade (pericardial effusion), and trauma.

The emergence of rapid response systems in human hospitals reflects a commitment to prevent CPA and improve survival in hospitalized patients. 7 Rapid response systems are designed to improve early recognition of deteriorating patient condition and cause an alarm to be triggered, eliciting an emergency mechanism that typically includes deployment of a rapid response team. This team includes personnel with special training in CPR, and its interventions include measures to prevent CPA. These types of systems have been successful in reducing IHCA rates. 7 In veterinary medicine, a rapid response system must be tailored to the individual practice in order to be meaningful, but should include both educational and infrastructural components (Appendix).

An in-hospital chain of prevention has recently been proposed as a means of increasing preparedness for and the quality of response to CPA in human patients. 43 The 5 key components of this chain are staff education, patient monitoring, recognition of a patient's deteriorating condition, the call for help, and the response. 32 Organization and communication among members of the health-care team are therefore critical for implementing effective preventative measures and responding to emergencies. In veterinary hospitals, particularly in a critical care environment, most of these components involve veterinary nurses and animal health technicians. This emphasizes their central role in establishing the first link in the chain of survival. In the authors' opinions, allocation of resources for continuing education of veterinary hospital staff, time for cage-side rounds, purchase of patient monitoring equipment, staffing for adequate monitoring of patients at risk for CPA, and an alerting mechanism to drive a rapid emergency response are important components needed to strengthen the first link in the chain of survival. However, veterinary data are currently lacking to substantiate the efficacy of prevention and preparedness measures for CPA in small animals.

The Second Link: Basic Life Support

Basic life support is the first strategy of action after CPA is identified. In the context of human CPR, this includes all components of life support that can be accomplished by trained and untrained rescuers, such as closed-chest compressions and mouth-to-mouth ventilation. Because CPR of veterinary patients typically occurs in a hospital setting where the equipment and skill to intubate patients are readily available, recommendations for basic life support include provision of a controlled airway, usually via ET intubation, and administration of chest compressions until additional personnel have arrived to add advanced resuscitation measures. Early initiation of high-quality basic life support is essential to create blood flow to the heart and brain as well as to limit injury to or preserve these organs until spontaneous circulation resumes.

Chest compressions—The advent of closed chest compressions more than 50 years ago revolutionized the treatment of CPA. 44 However, even optimal closed-chest CPR produces only 25% to 40% of normal cardiac output. 45,46 Similarly, CoPP, the driving force for myocardial blood flow, is only a fraction of the normal value during CPR. 47 Coronary perfusion pressure is calculated as the difference between aortic or arterial pressure and right atrial pressure during chest decompression. Sufficient coronary blood flow is essential for restarting the heart: in dogs used to study CPA and resuscitation, ROSC was unlikely and nonsurvival was predicted at a CoPP < 15 to 20 mm Hg. 46,48

Considerable size differences among dog breeds and the associated geometric and physical variations suggest that the technique for optimal chest compressions will vary according to these patient characteristics. 49 Furthermore, breed-specific variations in chest conformation influence the means by which blood flow is generated upon chest compression. The described mechanisms of compression-elicited flow include thoracic pump, cardiac pump, and a combination thereof. The primary characteristic of the thoracic pump mechanism is blood flow generated by increased intrathoracic pressure during chest compression; in this situation, the heart simply serves as a passive blood conduit. 50 Chest compressions in large dogs that have a rounded thorax (ie, barrel chest) will generate blood flow mostly by the thoracic pump mechanism. In contrast, the cardiac pump mechanism describes chest compressions that directly exert force on the heart and generate blood flow by changing the dimensions of individual cardiac chambers. The cardiac pump mechanism is favored by keel-shaped chest conformation, small size, and large amounts of chest-wall compliance (such as in cats) and is considered a much more effective means of blood flow generation than the thoracic pump. From a practical point of view, optimizing the thoracic pump effect would require hand placement over the highest point of the chest to achieve maximum reduction of chest volume (and thus maximum pressure increase) during each compression, whereas hand placement over the heart would likely be more effective in supporting the cardiac pump mechanism. Furthermore, high-velocity (high-impulse) compressions generate blood flow more consistently with the cardiac pump mechanism. 50 To further optimize direct cardiac compressions (ie, the cardiac pump mechanism) in cats, circumferential chest compressions are recommended in which the chest is compressed with both thumbs placed on the lateral aspect of the thorax directly over the heart and opposing force is applied with the tips of the fingers on the contralateral aspect of the thorax directly beneath the heart.

An age-related decrease in chest wall elasticity has been shown to impair blood flow during CPR in animals. 51 A more compliant chest wall may be responsible for predominance of the cardiac pump mechanism and for higher cardiac output during CPR of infants and immature animals, 52 and this could contribute to the substantially better outcomes reported after IHCA in infants, compared with findings for older children. 53 Cats have a high degree of chest wall compliance, compared with other species such as dogs, and chest compressions might therefore be assumed to be more effective; however, data to support this notion are not available in the literature. Lateral positioning for chest compressions is most reasonable for cats and all animals with a keel-shaped chest. In barrel-chested dogs, such as Bulldogs, sternal compressions are practically feasible and may be more effective, although this has not been examined. After the first few sternal compressions, dislocations in the costochondral junctions of the ribs typically occur and subsequently increase the efficacy of CPR as the cardiac pump mechanism contribution is increased.

Compression rate and duty cycle—In humans, a chest compression rate of 100 cpm has been recommended on the basis of results of investigations in non-human animals and on findings from a limited amount of clinical research indicating that a rate > 100 cpm is superior to a rate < 80 cpm, at least in adults. 54,55 The recommended compression rate of 100 cpm also applies to pediatric patients, despite the difference in body size. 56 Higher compression rates (eg, 150 cpm) evaluated during studies in dogs generally produced higher CoPP, greater cardiac output, and generally more favorable hemodynamics than did lower compression rates (60 cpm). 54,57 Conversely, excessively high compression rates could limit the duration of diastolic coronary perfusion and impair chest recoil or decompression, thereby compromising venous return. 58 Optimal chest compression rates in small animals are unknown, and results of a recent survey suggest that there is no consensus among veterinary practitioners in this regard. 59 During CPR in humans, rescuers typically deliver chest compressions too slowly, 13 and the most general recommendation is therefore to provide rapid compressions. However, the best evidence currently available indicates that rescuers should strive for a compression rate of 100 to 120 cpm in small animals. Duty cycle, or the ratio of compression time to decompression time, is recommended to be 1:1. 60

Compression force—In addition to the compression rate and duty cycle, optimization of compression force or compression depth is important for effective CPR. Coronary and cerebral perfusion pressures and blood flow are increased during high-force chest compressions, and the amount of force that can be applied is limited by the risk of CPR-associated injury. Complications that occur during standard CPR procedures in humans include rib fractures (13% to 97% of patients), pulmonary edema (44% to 46%), gastric dilation (29%), mediastinal hemorrhage (18%), aspiration (11%), pneumothorax (3%), and liver rupture (2%). 61,62 No comparable CPR-associated injury data are available for veterinary patients, although pulmonary and hepatic injuries have been reported in dogs under experimental conditions. 63 Despite the reported high incidence of CPR-related injury in humans, this is rarely a major contributor to outcome after CPA. 62 Compression depths of ≥ 5 cm (approx 2 inches) in adults and at least one-third of the anterior-posterior dimension of the chest in pediatric patients are recommended; however, it is very difficult for a rescuer to gauge compression depth while delivering CPR. 56,60 In veterinary medicine, considering the variation among species and breeds and the paucity of evidence to identify the optimal force under all these conditions, a general recommendation is to push hard.

Decompression—Complete chest recoil or decompression, which refers to passive expansion of the chest wall after a chest compression is delivered, is an important component of optimized CPR. Resuscitators often do not remove their weight from the chest after each compression, a circumstance referred to as leaning. 64 The consequences of leaning include increased intrapleural pressure, reduced venous return, and sub-optimal ventricular filling between compressions, all of which compromise efficacy of CPR. 65 It is therefore important to remove pressure after each compression to allow for proper recoil. Because fatigue may decrease chest compression rate and force and increase leaning, 60 it is recommended that rescuers performing compressions be replaced or switch positions with other team members every 2 minutes.

Interruption of chest compressions—Temporary discontinuation of chest compressions has been reported as a frequent and serious problem in CPR of human patients. 12,14 Unfortunately, resuscitators may be tempted to suspend compression activity in order to perform other tasks associated with CPR such as intubation, venous catheterization, ECG rhythm analysis, and pulse monitoring. In the absence of chest compressions, no blood flow is generated. Coronary perfusion pressure and CePP after a pause in compressions are lower than values just prior to the interruption, and it takes several compressions for perfusion pressures to return to preinterruption values. 66 Pauses have been shown to negatively affect outcome. 67,68 The AHA 2010 CPR guidelines emphasize the importance of minimizing these interruptions. 20,69 This recommendation is further supported by results of a recent study 70 in humans that showed a 14% decrease in survival to hospital discharge with every 5-second increase in chest compression pause intervals before and after defibrillatory shock. Moreover, limiting rhythm checks to once every 2 minutes is currently recommended, with uninterrupted chest compressions in between. 69 Rescuers are often unaware of the duration of these interruptions during CPR. It is therefore the responsibility of the CPR team leader to direct the CPR effort in a way to maximize effectiveness of compressions, limit the number of pauses to once every 2 minutes, and limit the duration of such pauses to < 10 seconds.

Interposed abdominal compressions—During CPR with interposed abdominal compressions, external midabdominal compressions are performed by a second rescuer. These added compressions are timed to take place between chest compressions. The preponderance of evidence from experimental studies in dogs indicates hemodynamic benefits of interposed abdominal compression. 71–74 It enhances the return of venous blood to the heart and increases intra-aortic diastolic (decompression) blood pressure and CoPP and thereby ameliorates myocardial blood flow. 71 Moreover, administration of these extra compressions increases carotid arterial blood flow, vital organ perfusion, and global oxygen delivery. 72,74 Broad application of interposed abdominal compression in humans has not been established because of conflicting clinical evidence, but reported complications in humans and dogs studied thus far are rare and not different from those associated with standard chest compressions. 63 Special circumstances such as the presence of diaphragmatic hernia, hemoabdomen, recent hepatobiliary surgery, or presence of gastric-dilation volvulus, if known, are contraindications. In the authors' opinions, in the presence of adequately trained rescuers and absence of specific contraindications, the use of abdominal compressions is reasonable.

Ventilation—Several studies 75–77 in which dogs and pigs were used to investigate OHCA have shown that ventilation during the first several minutes of CPR is not necessary. The limited importance of early ventilation can be explained by several mechanisms. 78 First, pulmonary oxygen uptake during the no-flow or low-flow states of CPA or CPR is very low. Second, reduced pulmonary blood flow allows an appropriate ventilation-to-perfusion ratio, even at low alveolar ventilation rates. Third, the lungs serve as a sufficiently large oxygen reservoir during the first few minutes of CPR when CPA is not caused by asphyxiation. Finally, chest compressions alone generate some degree of alveolar ventilation if an open airway is present. 79 There is ample evidence that excessive positive-pressure ventilation by the rescuers occurs frequently, reduces efficacy of CPR, and is harmful. 10 On the basis of this information and of recent clinical evidence in humans, and with the added intent of simplifying CPR by untrained bystanders, the AHA endorses compressions-only CPR for witnessed OHCA of presumed cardiac origin in human adults. 60,80,81 However, this recommendation does not apply to children or to individuals in which CPA is of noncardiac origin (eg, caused by apnea or asphyxiation). 60 Because CPA in most veterinary patients falls into the latter category, the recommendation for compressions-only CPR cannot be universally extended to veterinary practice. Therefore, during CPR, animals should always be ventilated as soon as possible, but chest compressions should not be withheld if an airway is not yet established.

Chest compressions should be initiated immediately upon recognition of CPA, as this will allow earlier initiation of blood flow with only minimally delayed ventilation. The previously recommended sequence A-B-C (Airway-Breathing-Circulation) is therefore altered to C-A-B. 60 Intubation should be performed by the most skilled person present to minimize the time required for task completion. It is then important to tie the ET tube in place and inflate the cuff. Intermittent positive-pressure ventilation can then be provided by use of a manual ventilation bag or with an anesthesia machine. The latter has the benefit that a manometer integrated into the machine allows determination of peak inspiratory pressure because intermittent positive-pressure ventilation should be limited in both rate and pressure. A ventilation rate of 10 breaths/min, with an inspiratory time of 1 second and a peak pressure of 20 cm H2O, is a reasonable recommendation for most small animal patients. This can be implemented by delivering a normal-sized breath (ie, a tidal volume of 10 to 15 mL/kg) with a short inspiratory time every 5 to 6 seconds. A more aggressive ventilatory regimen, including higher respiratory rates, peak inspiratory pressures, or positive end-expiratory pressure, is only acceptable in animals with severely impaired lung function, such as severe pulmonary parenchymal disease (ie, after pulmonary contusions). However, this is rarely necessary given the low degree of pulmonary blood flow during CPR. Chest compressions should not be interrupted to deliver positive-pressure breaths, and the breaths do not have to be synchronized with the compression phase (ie, compression or decompression of the chest). A reasonable practice is to use 100% oxygen for ventilation during CPR and to reduce Fio2 to maintain arterial oxygen saturation at ≥ 94% after ROSC to minimize the risk of oxidative injury during the reperfusion process while preventing hypoxemia. 82–84

Patient monitoring and assessment of quality of CPR—Adequate physiologic monitoring allows prompt identification of CPA in patients at risk, provides feedback on the efficacy of CPR, and helps to optimize patient care after CPA. Although monitoring during CPR provides feedback on the patient's response to resuscitation efforts, may cause adjustments in CPR technique, allows for recognition of ROSC, and may aid with prognostic evaluation, the intricacies of artificial circulation created by closed chest compressions limit the applicability of most of the familiar monitoring technology. The search for a suitable, noninvasive physiologic sensor that can be used to track the quality of circulation during CPR is ongoing. Intra-arrest monitoring is important for advanced as well as basic life support, and the information described here applies to both of the described chain-of-survival links.

Capnography—End-tidal CO2 values measured with capnography can be used to confirm correct ET tube placement and to assess efficacy of CPR. Under physiologic conditions, Petco2 serves as a close estimate of the alveolar partial pressure of CO2, which in turn is determined by a combination of CO2 production, pulmonary capillary blood flow (cardiac output), and alveolar ventilation. 85 Consequently, the use of Petco2 as a surrogate measure for chest compression–generated pulmonary blood flow is confounded by other variables, most importantly the amount of ventilation delivered. This suggests that minute ventilation should be held relatively constant when Petco2 is used as a qualitative measurement of CPR efficacy. However, special circumstances arise during CPR that may influence Petco2 values. Administration of epinephrine during CPR was shown to decrease Petco2 secondary to decreased cardiac output and pulmonary blood flow, despite having a positive effect on CoPP and on the rate of ROSC in human patients. 86,87 Sodium bicarbonate, occasionally administered during prolonged CPR as treatment against acidemia, is a nonmetabolic source of carbon dioxide that causes, if other factors are unchanged, a short-lived (1- to 2-minute) variable increase in Petco2. 88

Nevertheless, the results of several clinical and laboratory studies 45,89–94 have shown the value of Petco2 for monitoring CPR quality, and Petco2 is a very responsive and sensitive indicator that almost immediately increases upon ROSC. 90 Callaham and Barton 89 reported that an Petco2 < 10 mm Hg after 20 minutes of CPR in human patients who had an OHCA with pulseless electrical activity was 100% predictive for no ROSC. In the same study, 89 an initial Petco2 < 15 mm Hg (measured at the initiation of CPR) in patients following OHCA not caused by trauma was 91% predictive for no ROSC. In CPA caused by asphyxiation, initial Petco2 is expected to be higher, compared with values following arrest caused by VF, 95 and this initial value may not be a useful predictor for ROSC. 96

In a recent observational study 29 investigators evaluated peak Petco2 values during CPR in dogs and cats. Return of spontaneous circulation occurred in almost none of the dogs (1/18) that had a peak Petco2 < 15 mm Hg but was detected, at least temporarily, in most (25/29) of those for which the value was ≥ 15 mm Hg. Five of 9 cats with a peak Petco2 < 20 mm Hg did not have ROSC, whereas 9 of 10 with a peak Petco2≥ 20 mm Hg did have ROSC. On the basis of this information, possible guidelines for use of capnography to monitor CPR in dogs and cats are as follows: if initial Petco2 is 0, check the sensor and verify correct ET tube positioning; if Petco2 is < 15 mm Hg in dogs or < 20 mm Hg in cats, attempt optimization of the CPR techniques (eg, increase the pressure and frequency of compressions, avoid excessive intermittent positive-pressure ventilation, and attempt to identify reasons for ineffective CPR, such as pericardial tamponade or tension pneumothorax); if PETCo2does not increase to > 15 mm Hg in dogs or cats despite optimal CPR technique after 2 to 3 minutes, consider a different CPR method, such as open-chest CPR (depending upon the clinical situation); and if Petco2 remains < 10 mm Hg despite maximal effort and the ECG is not showing electrical activity, discontinuation of the resuscitation attempt can be considered.

Despite the low probability for ROSC when Petco2 values are very low, the results of a recent internet survey conducted by one of the authors (MB) suggest that the longest duration of CPR (mean ± SD) after which ROSC was achieved in veterinary patients was 25 ± 21 minutes when performed by general practitioners (n = 390) and 35 ± 14 minutes when performed by board-certified emergency and critical care or anesthesia specialists (61). Thus, it seems that continuation of CPR for ≥ 20 minutes would be meaningful before discontinuing resuscitation efforts, especially in the absence of Petco2 measurement capability. Initiation of open-chest CPR should not be delayed > 5 to 10 minutes after CPA in the face of ineffective CPR as indicated by Petco2 < 10 to 15 mm Hg because the risk for significant neurologic injury increases after that time. 97,98

Electrocardiography—An ECG allows determination of the arrest rhythm. In small animals, the most common arrest rhythm is asystole, but pulseless electrical activity, VF, and pulseless VT can also occur. Although the VT typically detected in clinical practice is a pulse-generating and perfusing rhythm, pulseless VT requires treatment identical to that for VF; thus, the rhythms are commonly referred to together as VF-VT. Rhythm identification is necessary for appropriate decision making in regard to medical management and defibrillation. 34,99 Although VF is an uncommon arrest rhythm in dogs or cats, it can develop during CPR after epinephrine administration. In humans, amplitude and frequency of VF have been used to prognosticate the likelihood of successful defibrillation 100 ; coarse (high-amplitude) VF with high frequency is an indicator of recent onset of CPA, and these patients have a higher probability of successful defibrillation. Fine (low-amplitude) VF with low frequency indicates global myocardial ischemia with a less promising outcome 99,101 but was shown to be reversible with CPR in studies of humans and nonhuman animals. 102 Electrocardiographic wave analysis for patients with VF has not been validated as a clinically useful method for assessment of the quality of CPR or as a predictor of successful defibrillation in veterinary medicine.

Blood pressure monitoring and pulse oximetry—Noninvasive blood pressure monitoring techniques, such as Doppler sphygmomanometry or oscillometric methods, are not useful tools to assess quality of CPR, but do have a role in postresuscitation care. Similarly, palpation of the femoral arterial pulse cannot be used to assess efficacy of chest compressions, partially because of the strong venous pulsation that occurs during CPR. 103,104 Arterial catheters are impractical to place during CPR, but if these are present, diastolic (relaxation) arterial blood pressure during chest recoil can be determined and CoPP can be estimated. 47 Assuming a relaxation right atrial pressure of 10 mm Hg, a relaxation arterial blood pressure of ≥ 30 mm Hg should be targeted to achieve a CoPP of ≥ 20 mm Hg, which is required for ROSC. 20,47,99 Mean and systolic arterial blood pressure readings are of uncertain value during CPR.

Pulse oximetry provides little meaningful information during CPR because arterial oxygen saturation is maximal in the majority of patients that have been intubated and ventilated with an Fio2 of 100%. Additionally, the quality of plethysmograms is impaired by peripheral vasoconstriction and motion artifacts.

Metabolic monitoring tools—Variables such as base excess values, blood lactate concentration, and central venous oxygen saturation allow insight into the severity of tissue hypoxia or the relationship between global oxygen delivery and oxygen consumption. Whereas base excess and lactate values lack the temporal resolution to allow for real-time quality assessment of CPR, continuous measurement of central venous oxygen saturation with a spectrophotometrical central venous catheter provides useful information on the efficacy of CPR and the likelihood for ROSC in humans 105,106 and may do so in dogs and cats as well. A drawback of this technology, in addition to the high cost of the catheter, is that central venous catheterization is necessary, whereby the catheter is advanced through the external jugular vein such that the tip resides in the intrathoracic cranial vena cava. 107 Some familiarity with central venous catheterization is necessary in order to perform this technique.

Monitoring CPR technique—Equipment designed to assess qualitative metrics of CPR performance, rather than the patient's physiologic response to CPR, is available. By use of accelerometers and thoracic impedance sensors, these feedback or prompting devices target optimization of the rate and depth of chest compressions as well as the rate of ventilation by instructing the rescuer via audiovisual feedback to push harder and faster. 108 Automatic recording of the CPR technique also allows for subsequent detailed debriefing. Investigations into the effects of these systems on the effectiveness of CPR in human patients showed a positive impact on the quality of CPR. 109,110 Even with the large variability in chest conformation in veterinary patients, these tools may prove useful for CPR optimization and debriefing because the general recommendations for compression and ventilation rate are similar in humans and small animals.

The Third Link: Advanced Cardiac Life Support

Advanced cardiac life support adds to basic life support measures to restore cardiac function. This component of the chain of survival comprises defibrillation, establishment of vascular access, administration of drugs, and open-chest CPR.

Defibrillation—Transthoracic defibrillation should be attempted for patients with VF or pulseless VT. Administration of high-quality chest compressions prior to the first defibrillation attempt increases defibrillation success because it causes some replenishment of myocardial energy stores. 21 Thus, high-quality CPR during defibrillator preparation with minimal pauses before and after delivery of the shock is essential. 20 Selection of the appropriate energy level for animal size and device (monophasic defibrillator, 5 ± 1 J/kg [approx 2.5 ± 0.5 J/lb]; biphasic defibrillator, 3 ± 1 J/kg [approx 1.5 ± 0.5 J/lb]) and minimization of impedance by creating optimal contact between the paddles and chest surface are important for successful defibrillation. 111 A common misconception is to immediately follow an unsuccessful defibrillation attempt with another attempt and to repeat this as many as 3 times, a technique known as stacked defibrillations. Each subsequent defibrillation is less likely to be successful, while concurrently, the hands-off time and therefore the period of no blood flow increases. Therefore, if a delivered shock fails to create a perfusing rhythm, chest compressions should immediately resume for about 2 minutes, followed by quick verification of a shockable rhythm and, if this is present, the next defibrillation attempt. This minimizes time without blood flow and reduces myocardial hypoxia, thereby increasing the chances for successful defibrillation with the subsequent shock. 20,67 Moreover, increasing the defibrillator dose of subsequent shocks by 50% once should be considered.

Methods for drug administration—Several possibilities exist for accessing the vascular compartment for the purpose of drug delivery during resuscitation. 107 The choice of drug administration routes during CPR is influenced by whether IV catheters are already placed and the anatomic locations of these, the number of personnel present and their technical skills, and the benefits and drawbacks of various vascular access methods. Characteristics such as delays in drug delivery to the central circulation (eg, aortic arch), drug peak plasma concentrations, duration of effective circulating drug concentrations, and risk of complications must be considered in determining the optimal route to use.

Peripheral venous access is generally uncomplicated and preferred by most veterinarians, 59 but the onset of effect of drugs delivered via this route is delayed, compared with that of drugs administered via a central venous catheter. 112 This delay can be minimized by subsequent bolus administration of an isotonic crystalloid fluid of ≥ 0.5 mL/kg (0.23 mL/lb) through the same peripheral vessel in which the drug was injected. 113 Administration of drugs via a cephalic vein leads to a shorter time to onset of drug effect than does administration via a saphenous or femoral vein. The external jugular vein can be catheterized by use of a cut-down technique, and the high jugular venous pressures generated by chest compressions facilitate identification of the vessel and counteract motion-related difficulties. Catheterization of the external jugular vein is easier and quicker for individuals who are accustomed with the technique, and this should be the preferred route of vascular access if no venous access has been established when CPA occurs. Moreover, the time until the drug reaches the central circulation is shortest and blood drug concentrations are highest when this route is used. 112

Intraosseous drug administration should be performed if venous access cannot be established promptly in pediatric patients, but this route can also be used in adult dogs and cats. Handheld electric IO drills are used for cannula insertion in adult and pediatric humans 114,115 and can be used in adult veterinary patients. Circulation time and peak circulating concentrations of drugs administered IO are reportedly comparable with those determined after administration through a peripheral vein. 116

Administration of drugs via the ET route offers a simple and rapid method for drug administration during CPR; however, it is not recommended as a primary route. Epinephrine, atropine, and vasopressin (but not sodium bicarbonate) can be administered via this route. The mnemonic device NAVLE (naloxone, atropine, vasopressin, lidocaine, and epinephrine) can be a useful reminder of CPR-related drugs that can be administered ET. At least 2 to 3 times the IV dose should be administered when this route is selected, and the drug should be diluted in an appropriate volume of saline (0.9% NaCl) solution (ie, 5 mL/20 kg [2.3 mL/44 lb] of body weight) and injected through a catheter that extends beyond the tip of the endotracheal tube. Distilled water may allow more effective absorption of the drug but can at least temporarily impair pulmonary oxygen exchange. 117 A downside to ET drug administration is that the dose-effect relationship is uncertain. 20 Furthermore, a depot-like effect can be caused by accumulation of epinephrine following ET administration during CPR when pulmonary blood flow is very low. This can lead to high serum concentrations of epinephrine, associated with protracted hypertension and tachyarrhythmias, after spontaneous circulation is restored and pulmonary blood flow increases. 118 The lack of proven clinical efficacy of drugs administered ET further indicates that this route should not be considered as a first choice. 119

Although used in small animal medicine, 59 transthoracic intracardiac injection of drugs is discouraged because of the risk of laceration of the aorta, pulmonary artery, or coronary artery; cardiac tamponade; pneumothorax; or intramyocardial injection. 120–123 In addition, targeted injection into the left ventricle appears impractical; only 11% and 3% of attempted intracardiac injections reached their intended goal in 2 studies 124,125 that used human cadavers to evaluate this procedure. Moreover, intracardiac injection necessitates interruption of chest compressions, and minimization of such interruptions is of paramount importance when considering routes of access for drug administration.

Vasopressor treatment—Other than medications used to counteract selected causes of CPA (eg, hypocalcemia, hyperkalemia, bradyarrhythmias, or anesthetic overdose), only compounds that increase peripheral vascular resistance have been shown to be of short-term benefit in the initial phase of CPR. The beneficial effect of vasopressor treatment is attributed to increases in CoPP and CePP because it is believed that these increase the rate of ROSC and the incidence of full neurologic recovery. 126 However, long-term survival benefits of vasopressor administration during CPR have not been proven in randomized clinical trials. 127,128 Epinephrine and vasopressin, both naturally occurring hormones, are the vasopressors most frequently used during CPR, although vasopressin is less commonly stocked than epinephrine in veterinary practices. 59 The vasopressor function of epinephrine is attributed to its α-adrenergic effects; however, it also exerts β-adrenergic effects and consequently increases myocardial oxygen consumption, is proarrhythmogenic, and contributes to postarrest myocardial dysfunction. 129–131 More recently, vasopressin (a nonadrenergic vasopressor) was identified as a promising and effective, if not superior, alternative to epinephrine in several studies 126,132–135 after IV, IO, and ET administration in various species. Recently, vasopressin was compared with epinephrine during CPR in dogs in a small randomized clinical trial, a and no additional benefit or increased risk was detected for any of the outcomes evaluated. A possible vasopressor regimen for dogs and cats after CPA could consist of rounds of initial low-dose (0.01 mg/kg [0.005 mg/lb], IV or IO) epinephrine, followed by vasopressin (0.8 U/kg [0.36 U/lb], IV or IO), and then another low dose of epinephrine, with 2 minutes of CPR in between drug administrations.

Drugs other than vasopressors—The anticholinergic compound atropine can be administered (0.05 mg/kg [0.023 mg/lb], IV or IO, or 0.1 to 0.15 mg/kg [0.045 to 0.068 mg/lb], ET) at initiation of CPR and repeated every 3 to 5 minutes in small animals with pulseless electrical activity or asystole arrest rhythms (most dogs and cats). This recommendation is predominantly based on an understanding of the pathophysiology of these arrest rhythms, which includes high vagal tone, rather than being founded on evidence. Lack of sufficient evidence for the effectiveness of atropine in humans with pulseless electrical activity or asystole arrest rhythms triggered its removal as a recommended drug from the 2010 AHA guidelines for CPR. 20 However, given the apparent lack of harm at recommended doses and the possible benefits suggested in some experimental studies 136,137 in dogs, it is the authors' opinion that atropine should be administered as part of the treatment for CPA in cats and dogs with pulseless electrical activity or asystole. Antiarrhythmic treatments, such as magnesium (30 mg/kg [13.64 mg/lb], IV or IO) for torsades de pointes arrhythmias or amiodarone (5 to 10 mg/kg [2.27 to 4.55 mg/lb], IV; first choice) or lidocaine (2 mg/kg [0.91 mg/lb], IV or IO, or 4 mg/kg [1.82 mg/lb] ET; second choice) for shock-resistant pulseless VT or VF, are rarely required in the setting of small animal CPR. 20,34

An effort should be made to treat underlying disease processes that may have contributed to CPA. If a component of hypovolemic shock is suspected, intravascular volume should be expanded accordingly with an appropriate IV fluid. 20 However, routine aggressive fluid administration for treatment of CPA is not recommended because this can increase right atrial pressure and thus compromise cerebral and coronary blood flow. 138 Similarly, routine administration of sodium bicarbonate during CPR is not recommended, but should be administered (1.0 mEq/kg [0.45 mEq/lb], IV) if severe metabolic acidosis (pH < 7.1) or hyperkalemia was present prior to CPA. 20 Calcium gluconate (50 mg/kg [22.7 mg/lb], IV or IO) should be given to patients in which pulseless electrical activity is a consequence of hypocalcemia, calcium-channel blocker toxicosis, or hyperkalemia, but should not be routinely administered without such circumstances because evidence for its benefit is lacking and hypercalcemic reperfusion can be injurious. 20,139 Glucagon (0.1 mg/kg, IV) may be effective if β-adrenergic receptor blocker or calcium-channel blocker toxicity caused the CPA. 20,140 If the patient is anesthetized when CPA develops, administration of sedatives, analgesics, and anesthetics should be discontinued and antagonists, such as naloxone (0.04 mg/kg [0.018 mg/lb], IV or IO; or 0.08 mg/kg [0.036 mg/lb] ET), flumazenil (0.01 mg/kg, IV or IO; or 0.02 mg/kg [0.009 mg/lb], ET), or atipamezole (0.05 mg/kg, IV), should be administered as appropriate.

Open-chest CPR—Patients that have CPA with cardiac tamponade, large-volume pleural effusion, or diaphragmatic hernia require open-chest CPR. Thoracocentesis, intercostal incision, or open-chest CPR is also required when CPA is accompanied by pneumothorax or tension pneumothorax. Transthoracic ultrasonography can be used for rapid identification of these conditions. 141,142 Open-chest CPR is also recommended when CPA develops intraoperatively with the chest or abdomen already open, and it should be considered after chest trauma with rib fractures. It is relatively contraindicated in animals with severe coagulopathy. Apart from the described circumstances, indications for open-chest CPR are the subject of debate, despite overwhelming evidence that proves the hemodynamic benefit of this procedure, which markedly increases or even normalizes cardiac output and coronary and cerebral blood flow, 97,98,143,144 compared with closed-chest CPR. No AHA recommendation has been made regarding this procedure in humans because of the lack of clinical studies that directly compare open-chest with closed-chest CPR procedures in humans. Consequently, the benefit-to-harm ratio cannot be assessed. 145 In contrast, veterinarians benefit from the large body of research conducted in dogs for experimental evaluation of CPR methods.

The duration of CPA before open-chest CPR is initiated is of critical importance. In an experimental study 97 of dogs with cardiac arrest, open-chest CPR resulted in ROSC after 10 and 20, but not 40, minutes of untreated CPA; however, none of the dogs for which the duration of CPA was 20 minutes survived to 24 hours after resuscitation. In another experimental laboratory study, 98 5 of 5 dogs (body weight, 28.5 ± 3.5 kg [62.7 ± 7.7 lb]) were successfully resuscitated by means of open-chest CPR after 5 minutes of untreated CPA and did not have functional neurologic deficits, whereas only 3 of 7 dogs treated by means of closed-chest CPR survived to the end of the study and none of these 3 were neurologically intact. In the absence of clinical veterinary studies to provide more guidance, it is reasonable to commence open-chest CPR no later than 5 to 10 minutes after CPA develops, especially in midsized to larger dogs (> 20 kg [44 lb] body weight) and barrel-chested dogs, in which closed-chest CPR is less likely to generate adequate blood flow. It is also reasonable to deliver open-chest CPR to any patient in which physiologic metrics of CPR efficacy indicate poor generation of blood flow (eg, Petco2 < 10 mm Hg) despite optimization of closed-chest CPR. In open-chest CPR, the heart is accessed through a left lateral thoracotomy in the sixth intercostal space. 146 Thoracotomy in itself is not expected to substantially influence outcome of the patient, but it demands additional resources for adequate surgical, analgesic, and intensive care support once ROSC has been established and stabilized.

The Fourth Link: Postresuscitation Care

Patient outcome is determined not only by the factors that led to CPA and durations of the no–blood-flow (CPA) and low–blood-flow (CPR) states, but also by physiologic and pathological processes during and after reperfusion. As a consequence, severe illness or death in patients that survive the immediate resuscitation phase can be attributed to post–cardiac arrest syndrome, defined as a combination of anoxic brain injury, postischemic myocardial dysfunction, the systemic ischemia and reperfusion response, and precipitating pathological changes 19,82 (Figure 2). Results of a large retrospective study 36 in humans revealed that approximately 44% of patients treated with CPR after an IHCA achieved ROSC, but only 39% of these individuals survived to discharge from the hospital. Hofmeister et al 29 reported that only 16% of dogs and cats that had an ROSC after IHCA and CPR survived to discharge from the hospital. Thus, a number of lives could be saved during the immediate period following CPR. The importance of the postresuscitation phase has recently been emphasized, and a part of the 2010 AHA CPR guidelines is dedicated to this subject. 19,21,82

Figure 2—
Figure 2—

Flow chart depicting pathophysiology, clinical manifestations, and potential treatments for the 4 major components of post–cardiac arrest syndrome. ARDS = Acute respiratory distress syndrome. CHF = Congestive heart failure. ECMO = Extracorporeal membrane oxygenation. MODS = Multiorgan dysfunction syndrome. PCAS = Post–cardiac arrest syndrome. PTE = Pulmonary thromboembolism. SIRS = Systemic inflammatory response syndrome. Modified from Neumar et al. 19

Citation: Journal of the American Veterinary Medical Association 240, 5; 10.2460/javma.240.5.540

Post–cardiac arrest brain injury—Autoregulation of cerebral blood flow may be impaired, and an adequate CePP (eg, ≥ 60 mm Hg) requires a mean arterial pressure of ≥ 80 mm Hg. 147 Neurologic function is of particular concern after CPA, given the vulnerability of the brain to ischemia and the secondary brain injury that occurs during reperfusion. 82,148 However, the positive effect of mild therapeutic hypothermia on neurologic outcome in humans, even when started hours after ROSC, clearly shows that the therapeutic window to alleviate some of this brain injury is much wider than expected. 16,17,82

Mild therapeutic hypothermia is an accepted and progressively more common component in the care of humans that remain comatose after resuscitation from CPA. 82 It involves cooling to a target (esophageal or bladder) core temperature of 32 to 34° C (89.6° to 93.2°F). This is performed by means of clinically used technologies such as surface cooling blankets or endovascular cooling catheters and can also be accomplished simply with ice-cold IV infusions or application of ice packs. 149 Reaching target temperature as soon as possible after reperfusion (ROSC) is likely important. 150 The optimal duration of mild therapeutic hypothermia is not yet clear, but the current AHA recommendation is 12 to 24 hours in humans. 82

Whether therapeutic hypothermia is a feasible and effective strategy to use in initially comatose veterinary patients needs to be examined because management and monitoring efforts may be considerable. However, the effort appears to be commensurate with that needed for long-term mechanical ventilation. Early clinical reports 151,152 have already described the use of mild therapeutic hypothermia as an adjunctive treatment for traumatic brain injury in a dog and use of deep hypothermia during open heart surgery in dogs. Permissive hypothermia (ie, allowing the animal to slowly rewarm to normal body temperature for many hours after CPA without attempting to raise its temperature by other means) could be a more realistic variant for veterinary patients. Although the full potential of therapeutic cooling may not be realized with this permissive approach, the harmful effect of rapid active rewarming may be attenuated: in humans, the currently recommended rewarming rate after mild therapeutic hypothermia is 0.25°C (0.45°F)/h and faster rewarming may be injurious. Fever or overshoot hyperthermia during rewarming must be prevented. 82,153–158

Mechanical ventilation may help to prevent rearrest in patients in which brainstem injury prevents adequate autonomous control of ventilation or in which respiratory failure was a precipitating factor for CPA. Continued mechanical ventilation is the safest method to consistently assure appropriate oxygenation (oxygen saturation as measured via pulse oximetry, ≥94%; Pao2, approx 100 mm Hg) at minimum Fio2 and optimal ventilation (Paco2, approx 40 to 45 mm Hg; Petco2, approx 35 to 40 mm Hg); it also allows medical personnel to focus their attention on hemodynamic optimization. 82 Under physiologic conditions, autoregulation of cerebral blood flow allows for a constant cerebral blood flow over a large range of arterial blood pressures. However, after global cerebral ischemia, this control can be lost and blood flow becomes directly dependent on CePP. 159 Thus, adequate CePP is of particular importance after global cerebral ischemia, and the cardiovascular instability that commonly occurs after CPA needs to be proactively addressed.

A CPA-associated increase in intracranial pressure is uncommon in humans, 19,160 and this is likely to be true in dogs and cats as well. To the authors' knowledge, mannitol administration during or after CPR has not been studied; therefore, there is little reason to recommend its routine use during the postresuscitation phase. However, if an increased intracranial pressure is suspected on the basis of clinical signs, pre-existing disease, or results of diagnostic imaging (eg, CT scan), mannitol (0.5 to 1.0 mg/kg [0.23 to 0.45 mg/lb]) or hypertonic saline (7% NaCl) solution (3 mL/kg [1.36 mL/lb]) should be administered IV Hypoxia, hypocapnia or hypercapnia, and hypotension should be prevented to allow adequate oxygen delivery to the brain. Also, seizures need to be aggressively controlled because they can be detrimental to neurologic recovery. 19

Myocardial dysfunction—Clinicians must be prepared to encounter low cardiac output states in patients after CPR. These states are caused in part by systolic and diastolic dysfunction secondary to myocardial stunning (which is often further complicated by ventricular tachyarrhythmias). 161,162 The term myocardial stunning reflects the transient nature of left ventricular dysfunction, in contrast to other cardiac conditions such as myocardial infarct. 162 Left ventricular function and cardiac rhythm can be expected to improve within 48 hours after ROSC, depending on the nature and severity of ischemic injury. 161,163 Positive inotropes such as dobutamine (5 to 15 μg/kg/min [2.27 to 6.82 μg/lb/min], IV) can be used to treat left ventricular dysfunction during the postresuscitation phase. 164 The degree of left ventricular dysfunction and the effects of positive inotropes can be objectively and serially assessed with the use of transthoracic echocardiography. 141,162 Human data also suggest that transthoracic echocardiography may be useful in assessing a patient's fluid status during the postresuscitation phase. 165

Systemic ischemia-reperfusion response—The hemodynamic status of patients at the macrocirculatory and microcirculatory levels may be further complicated by a plethora of postresuscitation processes that are phenotypically similar to those described in patients with sepsis. 166 Increased circulating concentrations of inflammatory mediators, myocardial dysfunction, vasoplegia, relative adrenal insufficiency (ie, circulating corticosteroid concentrations and responses that are inadequate for the degree of physiologic stress), coagulation abnormalities, and microvascular dysfunction including increased vascular permeability have all been reported in patients after CPR. 131,161,166–171 A hemodynamic optimization strategy 19 comparable with that described by Rivers et al 172 for early goal-directed treatment of sepsis and septic shock is herein recommended for the treatment of small animal patients with this sepsis-like syndrome during the postresuscitation phase. Global hemodynamic and perfusion variables should be used as endpoints, with IV fluids, vasoactive and positive inotropic drugs, and blood products administered as needed to reach optimized mean arterial and central venous blood pressures, urine output, hemoglobin concentration, and venous oxygen saturation. 82,172,173

Other postresuscitation concerns—The patient's precipitating disease may further complicate the treatment regimen, as will organ dysfunction such as ileus and renal injury. Given the complexity and diverse nature of the abnormalities that develop after CPA, a treatment protocol that unites several therapeutic strategies, rather than a single intervention, is necessary. Results of human studies 173,174 have revealed that implementation of a standardized, comprehensive postarrest treatment protocol can improve rates for discharge from the hospital and for survival with good neurologic outcome. Treatment elements in those studies included therapeutic hypothermia, strict glycemic control, goal-directed hemodynamic optimization, and percutaneous coronary intervention; the relative contribution of each individual element remains uncertain. 127 The value of a comprehensive postresuscitation care plan for veterinary patients has not been established, but referral to a veterinary specialty center that can provide advanced 24-hour specialty care and intensive monitoring is reasonable, especially for patients that remain comatose or hemodynamically unstable or have other severe disease. Such centers should have the capacity to provide continuous hemodynamic assessment (including arterial and central venous blood pressure measurement), blood gas analysis, assessment of acid-base status, mechanical ventilation, parenteral nutrition, blood product administration, and monitoring and control of body temperature. However, safe transport of critically ill pets to a tertiary care veterinary hospital is problematic. Commercial veterinary ambulance services may be available in some areas, but most veterinarians are likely to have limited access to such services.

It is clear that adequate postresuscitation care is of vital importance to realize the best possible outcome for animals after CPA. It is also evident that the required critical care can be long in duration, expensive, and associated with an uncertain outcome. In many situations, the cost of optimal care may be prohibitive for pet owners. It is for this reason that a focus on the recognition of risk factors for CPA and preemptive care is of utmost importance.

Conclusions

A comprehensive chain of survival that starts with recognition of risk factors for CPA and reaches far into the postresuscitation phase is necessary in order to improve outcomes for small animals with CPA. There are several special conditions in veterinary medicine that make this type of care more challenging, such as limitations in resources and trained personnel and pet owner willingness and ability to commit to the long-term and intensive care that is needed for many of these patients. Thus, prevention of CPA and early recognition of the patients imminently at risk are of vital importance, and underlying risk factors or metabolic abnormalities need to be corrected. Once CPA develops and CPR is initiated, early and effective chest compressions and airway management will help to minimize the duration of ischemia and to limit the severity of postresuscitation complications. If CPR leads to stable ROSC, referral to a specialty center that can provide advanced 24-hour care and intensive monitoring should be considered to optimize outcome.

ABBREVIATIONS

AHA

American Heart Association

CePP

Cerebral perfusion pressure

CoPP

Coronary perfusion pressure

CPA

Cardiopulmonary arrest

cpm

Compressions per minute

ET

Endotracheal

Petco2

End-tidal partial pressure of carbon dioxide

Fio2

Inspiratory oxygen fraction

IHCA

In-hospital cardiac arrest

IO

Intraosseous

OHCA

Out-of-hospital cardiac arrest

ROSC

Return of spontaneous circulation

VF

Ventricular fibrillation

VT

Ventricular tachycardia

a.

Buckley GJ, Rozanski EA, Rush JE. Randomized blinded comparison of epinephrine and vasopressin for the treatment of naturally occurring cardiopulmonary arrest (CPA) in dogs (abstr). J Vet Intern Med 2011;3:646

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Appendix

Key elements of a veterinary rapid response system to systematically prevent in-hospital CPA and to optimize response to CPA.

  • • Systematic staff education on patient deterioration and its detection.

  • • Systematic identification of patients at risk during cage-side rounds.

  • • Frequent monitoring of vital signs and assessment of at-risk hospitalized patients.

  • • Definition and consistent use of criteria for notification of clinicians for at-risk patients.

  • • A notification system of calling for assistance.

  • • Rapid and effective clinical response to calls.

  • • Debriefing after each event.

  • • Systematic evaluation of performance measures and continuous quality improvement.

Modified from Bhanji et al. 7

  • Figure 1—

    Schematic illustration of the chain of survival for small animals symbolizing the continuum of care required to successfully manage CPA.

  • Figure 2—

    Flow chart depicting pathophysiology, clinical manifestations, and potential treatments for the 4 major components of post–cardiac arrest syndrome. ARDS = Acute respiratory distress syndrome. CHF = Congestive heart failure. ECMO = Extracorporeal membrane oxygenation. MODS = Multiorgan dysfunction syndrome. PCAS = Post–cardiac arrest syndrome. PTE = Pulmonary thromboembolism. SIRS = Systemic inflammatory response syndrome. Modified from Neumar et al. 19