Andrea Monnig, DVM, DACVECC
Cardiopulmonary arrest (CPA) is the abrupt and complete failure of the respiratory and circulatory systems, which leads to cessation of blood flow, tissue hypoxia and cell death. Studies have reported survival to discharge rates ranging from 3 – 6% in dogs and 2.3 – 9.6% in cats. Animals that arrest under general anesthesia have the greatest likelihood of regaining return of spontaneous circulation (ROSC) and survival to discharge. With such grim success rates, it is important to identify predisposing causes of CPA in an attempt to treat the underlying cause and ward off impending arrest. Some predisposing factors include hypovolemia, hypoxemia, acidosis, hypo- or hyperkalemia, hypo- or hyperthermia, toxins, trauma, tamponade and pneumothorax.
In the event of an arrest, preparedness of the veterinary team is of utmost importance. A readily available, well-stocked (routinely audited) crash cart located in patient care areas is recommended. Effective communication through designation of a team leader with delegated tasks to individual team members will ensure that protocol is followed. Debriefing staff on CPR performance, problems involving equipment or drugs, or other issues that may arise can improve the overall quality and potential outcome of future codes.
Basic life support (BLS) involves the recognition of CPA, initiation of chest compressions, airway management, and the provision of ventilation.
One of the greatest factors in CPA outcome is the quality of chest compressions. The vast difference in size and conformation of thoracic cages of our patients precludes recommendations for hand position at a single location. For cats, small dogs and keel-chested dogs, the preferred method is the cardiac pump mechanism, in which hands are placed directly over the heart. In medium to giant breed dogs with rounded chests, direct compression over the heart is unlikely to be effective. Recommended for these animals is the thoracic pump mechanism, where compressions are delivered over the widest portion of the thorax. The thoracic pump mechanism relies upon alterations in intrathoracic pressure to create forward flow. During thoracic compression there is an increased intrathoracic pressure, which causes a secondary compression of the aorta and vena cava leading to blood flow out of the thorax. During elastic recoil of the chest wall, the intrathoracic pressure becomes negative acting as a vacuum drawing blood from the periphery back into the thorax.
Recommended compression rate is 100-120/min in dogs and cats. Compressions should be performed by a person standing above the patient, with the elbows locked, bending at the waist. Compression depth of 1/3– ½ the width of the thorax in a 1:1 compression:relaxation ratio, permitting full elastic recoil of the chest is the key to good form. Recognition of compressor fatigue is important, as rate and depth of chest compressions decrease over time. Chest compressions should be performed for 2 minutes, unless signs of fatigue are recognized.
Ideally, ventilation is provided through endotracheal intubation. Non-invasive techniques such as mouth-to-snout or a tight fitting mask may be acceptable alternatives. Ventilation rates are recommended at 10 breaths per minute, 10 ml/kg tidal volume, and 1 second inspiratory time. Increased respiratory rates, tidal volumes and inspiratory times can lead to increased intrathoracic pressure, decreased venous return and decreased perfusion.
Advanced life support (ALS) includes vasopressor therapy, positive inotropes, anticholinergics, electrical defibrillation, antiarrhythmics and other miscellaneous interventions including correction of acid-base and electrolyte disorders and resolution of volume deficits.
Drug therapy is a staple of ALS. Epinephrine and vasopressin are the most common vasopressors used during CPR. Vasopressor therapy increases systemic vascular resistance increasing the cardiac output that remains within central circulation. Two doses of epinephrine have been reported for the treatment of CPA, the low dose (0.01 mg/kg IV) and the high dose (0.1 mg/kg IV) dosed every 3-5 minutes. Although the high dose has been associated with increased ROSC, it does not necessarily increase survival to discharge. High dose epinephrine may be considered for repeat dosing or prolonged CPR. Vasopressin, a nonadrenergic vasopressor, acts on vascular smooth muscle. The benefits of this drug as a vasopressor include efficacy in the face of acidosis and no inotropic or chronotropic effects, which may worsen myocardial ischemia. Epinephrine and vasopressin may be used interchangeably. Increased vagal tone is thought to be a predisposing condition to CPA in small animal veterinary patients. Routine use of atropine (0.04 mg/kg IV) in dogs and cats can be considered.
The most common arrest rhythms identified in veterinary patients include asystole, pulseless electrical activity (PEA) and ventricular fibrillation (VF). There is no proven drug therapy for asystole or PEA. Electrical defibrillation is the most effective therapy against VF and pulseless ventricular tachycardia (VT). Antiarrhythmic agents, including amiodarone, lidocaine and magnesium, have been investigated for the treatment of VF/pulseless VT. Amiodarone is the only drug that has consistently demonstrated a benefit in these cases. Lidocaine is an alternative if amiodarone is not available, but it may increase the defibrillation threshold for conversion. There is insufficient evidence to support the routine use of magnesium.
Other drug therapies to consider during CPA include reversal agents, electrolyte therapy, alkalinization therapy and corticosteroids. Reversal agents such as naloxone, flumazenil or yohimbine/atipamezole can be administered if there is reason to believe that its counterpart drug played a role in the patient’s arrest. In the face of documented ionized hypocalcemia administration of Ca2+ may be beneficial in skeletal and smooth muscle function. Hypokalemia should be documented prior to treatment with potassium-containing drugs. Sodium bicarbonate (NaHCO3) therapy is not recommended for routine use during CPR. Corticosteroids have been investigated in both experimental and clinical studies. There is no demonstrated benefit from corticosteroids, and there is a potential for harm following high-dose administration. Thus, the routine use of steroids is not advised. IV fluids are only indicated in hypovolemic patients.
Monitoring during CPR should include ECG and ETCO2. ETCO2 can be used as an early indicator of ROSC as it assesses perfusion of the alveolus rather than ventilation. Dogs whose ETCO2 > 15 mmHg and cats ETCO2 > 20 mmHg may have an increased rate of ROSC. Electocardiographic monitoring during intercycle pauses of chest compression will allow for appropriate ALS therapy based upon rhythm diagnosis. However, chest compressions should not be stopped to assess the ECG in between theses cycles. Palpation of pulses is not an effective means of monitoring during CPR. Chest compressions should not be held so one can attempt to palpate pulses. Corneal Doppler is not recommended because it can be complicated by motion artifact and retrograde venous flow.
Following a successful resuscitation, intensive care is required. Patients should be optimized hemodynamically, respiratory function managed in an effort to target normoxia and normocapnia, and interventions provided to protect neurologic function.