Introduction

The overall incidence of cardiopulmonary arrest (CPA) during anesthesia or sedation in veterinary medicine is reported to be 0.17% in dogs and 0.24% in cats [1]. While the overall survival rate from CPA is 6–7% [2], the survival rate for dogs and cats that have CPA while anesthetized is as high as 47% [3]. Guidelines for cardiopulmonary resuscitation (CPR) in veterinary medicine have historically been determined by guidelines from human medicine, specifically by the American Heart Association (AHA) or have been developed based on veterinary expert opinion [4]. The Reassessment Campaign on Veterinary Resuscitation (RECOVER) has developed guidelines for CPR in dogs and cats and was also designed to increase our knowledge to improve the quality of these guidelines for CPA [5–11]. This chapter is based on the RECOVER guidelines for CPA in dogs and cats and is directed to CPA in the perianesthetic period.

CPR Preparedness and Prevention

The most important element of having an efficient CPR experience is to have a premade arrest station, or crash cart, that contains all of the items necessary for CPR (Figures 23.1–23.5) [4]. The crash cart should be organized in a manner that all essential equipment can readily be obtained from the cart during a CPR event. The example provided has the biphasic (BP) veterinary defibrillator with electrocardiogram (ECG) cables, attached pulse oximeter, ECG pads, and suction unit on top of the crash cart (Figure 23.1). The first drawer contains various sized syringes with and without needles, catheter flush, and CPR drugs (Figure 23.2). The second drawer contains airway management items including a portable capnometer (Figure 23.3). The third drawer contains IV catheter items (Figure 23.4). The fourth drawer contains surgical items and the internal defibrillation paddles (Figure 23.5). The crash cart should be in an area that is readily accessible during the perianesthetic period, whether it is in the main treatment area, in an induction or surgical suite, or in the recovery area. The most common problem in human medicine involving the arrest station area is lack of returning equipment or not restocking necessary medication [12]. Therefore, some indicator such as a piece of intact tape needs to be placed on the crash cart to know that it is fully stocked, marked with date it was updated (Figure 23.1).

There is essential equipment for a crash cart (Table 23.1) including multiple sizes of needles, syringes, and IV catheters along with ready‐made securing material. There should be a variety of endotracheal tubes and equipment to secure an airway, including materials to perform an emergent tracheostomy. CPR drugs are discussed later in the chapter. A defibrillator with an ECG monitor is the most expensive yet essential item in a crash cart, since no currently available drugs will effectively and reproducibly convert ventricular fibrillation (VF) to normal sinus rhythm; only electrical defibrillation can convert VF. Suction should also be readily available.

Human evidence suggests that the quality of CPR improves with continued training and the use of CPR manikins [13]. There are no current studies in veterinary medicine that investigate the effect of training, or lack of continued training, on the effectiveness of CPR. Most veterinarians and veterinary nurses learned CPR during their initial schooling and many personnel may have minimal experience with CPR unless working in an emergency environment. It is recommended that veterinary personnel review all equipment (including the defibrillator) and CPR protocols and procedures every 6 months [11]. This is especially true for anesthesia personnel considering that CPR for an anesthesia or sedation event has a higher chance of being successful [7]. Veterinarians and veterinary support staff can obtain CPR certification through the RECOVER website (www.recoverinitiative.org).

Defibrillator with ECG capability—both external and internal paddles, gel for external paddles Intubation equipment—several sizes of endotracheal tubes, laryngoscope, several sizes of laryngoscope blades, material to tie in endotracheal tube Ambu bag—two sizes Drugs: epinephrine, atropine, lidocaine, naloxone, flumazenil, atipamezole Intravenous catheter material Surgical equipment for open chest cardiac massage Tracheostomy equipment

Drug	Heart rate	Blood pressure	Respiratory effect
Opioids (e.g., morphine, hydromorphone, methadone)	Bradycardia, AV block	No direct effect, though hypotension with bradycardia	Moderate depression
Alpha‐2 agonists (e.g., dexmedetomidine)	Bradycardia, AV block	Increase or decrease	Moderate depression
Acepromazine	Tachycardia	Hypotension	No effect
Propofol	Tachycardia	Hypotension	Severe depression
Alfaxalone	Tachycardia	Hypotension	Severe depression
Benzodiazepines	Minimal effect	Minimal effect	Mild depression

AV, atrioventricular.

A CPA related to anesthesia or sedation has a high likelihood of being prevented. Many anesthetic drugs are cardiopulmonary depressants and are commonly used in combination, resulting in additive or synergistic decreases in cardiac and pulmonary functions (Table 23.2). Constant monitoring during anesthesia can result in recognition of early signs of CPA (see the section titled “Basic Life Support” in the following text) and early intervention. An important advantage to several anesthetic drugs is reversibility. For example, atipamezole reverses the effects of dexmedetomidine, naloxone reverses opioid effects, and flumazenil reverses benzodiazepine action. In addition, 100% oxygen is delivered during inhalation anesthesia and some method of oxygen delivery can be applied during sedation. It is possible that the increased survival rate for CPR in anesthetized patients could be due to higher arterial oxygen content before CPA and an increased time before tissues such as the brain and heart become hypoxic. Another possible reason for a higher success rate in anesthetized animals undergoing elective procedures is that some anesthetized patients tend to be younger in age.

Basic Life Support

Basic life support (BLS) is defined as the recognition of CPA, obtaining a patent airway, and performing ventilation and chest compressions (external or internal) [7]. Human studies suggest that the BLS quality is directly related to an increased survival rate [14, 15]. Chest compressions can be either external or internal with external chest compressions utilized far more commonly. The indications for immediate internal compressions, also termed cardiac massage, include a thoracic cage that is not intact, usually due to trauma, or if the patient is under general anesthesia during an abdominal or thoracic surgery.

With CPA during inhalation anesthesia, the most challenging aspect of BLS will be recognition of CPA, as patients are already intubated, usually have patent IV catheters with fluids being administered, and are receiving 100% oxygen. There are no studies that address the issue of recognizing CPA in anesthetized dogs and cats [7]. Identification of CPA in nonanesthetized dogs and cats involves loss of consciousness, lack of breathing efforts or agonal gasps, and/or loss of a heartbeat or pulse [7]. Other signs indicative of CPA include pale to white mucous membranes and sudden loss of blood pressure. These signs can be applied to dogs and cats that are sedated. However, identification of CPA during inhalation anesthesia can be more challenging and may be dependent on the amount of monitoring being used. Inhalation anesthetics are potent respiratory depressants, and it is expected for dogs and cats under inhalation anesthesia and breathing spontaneously to have reduced respiratory rate/tidal volume and increased arterial carbon dioxide as measured by arterial blood gas or via capnography. Cessation of all respirations (respiratory arrest) is usually followed by cardiovascular complications such as severe bradycardia and hypotension and developing sinus arrest or VF. Breath by breath decreases in end‐tidal carbon dioxide (ETCO₂) are a sign of impending circulatory arrest and complete, abrupt cessation of ETCO₂ can signify cardiac arrest [16].

Sedated dogs and cats that experience CPA should have an airway secured and ventilation begins at 10 breaths min⁻¹ via an Ambu bag or anesthesia machine while chest compressions are started [7, 11]. Immediate ventilation is essential in BLS, as studies in animal models and human clinical patients show that hypoxia and hypercapnia reduce the likelihood of return of spontaneous circulation (ROSC) [17, 18]. Care should be taken to avoid hyperventilation; therefore, in addition to a rate of 10 breaths min⁻¹, an inspiratory time of 1 s should be applied, as this time equates to a tidal volume of approximately 10 ml kg⁻¹ [7].

External chest compressions should begin immediately. High‐quality external chest compressions can provide a maximum of 25–30% of the normal cardiac output; animal position and hand location are extremely important to achieve this goal (Figures 23.6 and 23.7) [11]. The two theories of circulation during external chest compressions are the cardiac pump theory and the thoracic pump theory. One experimental study has revealed the difference between the cardiac and thoracic pump theories of external chest compressions [19]. For example, external chest compressions over the heart result in closure of the mitral valve and direct blood flow from the heart (cardiac pump). External chest compression directed at the peak height of the thorax in lateral recumbency results in the mitral valve continuously open and blood flow circulating passively (thoracic pump). There is a difference in recommended hand placement based on the size of the dog or cat (Figures 23.6 and 23.7). A medium‐ to large‐sized dog should have the back against the resuscitator and both hands placed at the highest part of the thorax (Figure 23.6). The thoracic pump theory is likely to prevail with this method of external chest compressions. Small dogs and cats can be placed perpendicular to the resuscitator with one hand over the thorax and one had over the sternum (Figure 23.7). Both hands compress simultaneously, as one hand will be directly over the heart and one hand will be at the highest part of the thorax. The cardiac pump theory is likely to occur during compressions using this method. Dogs with a thorax that is equally deep as wide can be in lateral or dorsal recumbency during external chest compressions, though this technique may seem uncomfortable.

The external chest compression rate in dogs and cats necessary for maximal cardiac output is between 100 and 120 beats min⁻¹ [7, 11]. The ideal depth of external chest compressions has not been determined in dogs and cats. However, extrapolation from human CPR studies implies that a depth between one‐third and one‐half of the chest wall width is reasonable, whereas greater than one‐half of the depth could damage the thoracic wall [20]. Allowing complete thoracic recoil is vital to maintain cardiac output during external chest compressions; leaning on the thorax during chest compressions in humans decreases cardiac output [21]. In addition, there should be no pause in external chest compressions when delivering breaths during CPR [7, 11]. Finally, mixed results are seen in dog and pig models concerning interposed abdominal compression with external chest compression to improve venous return and cardiac output [7]. No harm has been shown with interposed abdominal compressions, though a large benefit has not been seen; thus, while this technique may not be detrimental, it may not be advantageous and yet requires a second resuscitator to perform.

A realistic clinical factor during CPR when maintaining effective external chest compressions at 100–120 beats min⁻¹ is rescuer fatigue, especially in large dogs. Human CPR studies using manikins revealed a loss of external chest compression quality over the first three minutes [22]. Recommendations for veterinary CPR are to change resuscitators every two minutes [7, 11].

The next step for CPR in a sedated dog or cat is to reverse any previously administered opioid or alpha‐2‐adrenergic agonist. The benzodiazepines produce minimal cardiac or pulmonary depression and may not need to be reversed, especially since seizures may occur during the postresuscitative period. Although naloxone has a very short duration of action and may be administered multiple times, atipamezole has a very long duration of action and likely will not need to be given more than once.

Decisions to either continue with advanced life support (ALS) CPR, administer electrical defibrillation, or to discontinue CPR due to ROSC should be made based on monitoring, discussed in the following text. The ECG will be an important monitor, as the electrical activity of the heart will determine how to proceed with ALS [7].

Advanced Life Support

ALS is defined as all resuscitative efforts after BLS that can include drug administration, correction of volume deficits and electrolyte abnormalities, blood product administration, and electric defibrillation [8]. The ALS domain of the RECOVER initiative determines aspects of ALS that have historically been very controversial, based on individual bias and experience, or extrapolated directly from human CPR. The most important ALS aspects directed to veterinary patients include the treatment of asystole, pulseless electrical activity (PEA), VF, vasoactive and cardioactive drug use, and supplemental treatment implementation (i.e., oxygen, fluid therapy, blood products administration, and correction of electrolyte disturbances) in an attempt to not only make species‐specific recommendations but also to simplify the technique of veterinary CPR.

Primary CPR drugs intensely investigated are epinephrine and atropine. Anecdotally, many veterinarians were taught to co‐administer atropine first then epinephrine second as a standard initial drug therapy during CPR. However, there is an inherent danger to this practice, as atropine lowers the VF threshold in experimental models [23]; increased vagal tone can be protective of VF [24]. No specific experimental studies address the concurrent administration of atropine followed by epinephrine as a standard first line of drug therapy for CPR. The clinical importance is that if no defibrillator is available for CPR and VF occurs, there is no drug therapy to correct VF. Also, many anesthetic drugs increase vagal tone and bradyarrhythmias. Decision‐making during an arrest where a patient has received these anesthetic drugs can also be very important, as atropine takes 1–2 min to produce an effect and epinephrine takes seconds to work.

Epinephrine is a vasoactive drug with positive chronotropic and inotropic effects that provides increases in coronary perfusion, heart rate, and blood pressure. After extensive research, the recommended dose of epinephrine for veterinary patients is 0.01 mg kg⁻¹, IV [8]. Past human experimental and clinical studies investigated the “high” dose of epinephrine (0.1 mg kg⁻¹, IV) compared to the “low” dose of epinephrine (0.01 mg kg⁻¹, IV); children receiving “high”‐dose epinephrine compared to “low”‐dose epinephrine had lower survival rate [25]. There have been no studies in dogs and cats comparing “high”‐ and “low”‐dose epinephrine [8].

A possible alternative to epinephrine is vasopressin (0.8 U kg⁻¹

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