The success of cardiopulmonary resuscitation (CPR) efforts depends on many factors, including the underlying cause of the arrest, the timeliness and effectiveness of the intervention, and the preparedness of the team administering CPR. Overall prognosis of recovery from cardiopulmonary arrest (CPA) with CPR efforts is as high as 35%–44%; however, only <10% of animals survive to discharge. Animals with CPA associated with anesthesia have a better prognosis. The American College of Veterinary Emergency and Critical Care developed the first set of guidelines for veterinary CPR; this effort was termed the Reassessment Campaign on Veterinary Resuscitation (RECOVER) and is available on the association's website at www.acvecc-recover.org. CPR is divided into several sections: prevention andpreparedness; basic cardiac life support (BCLS) promoting oxygenation, ventilation, and circulation; advanced cardiac life support (ACLS) using electrocardiographic evaluation of cardiac rhythms, administration of drugs, and defibrillation when necessary; monitoring during CPR; and postresuscitation management, which involves intensive monitoring of common complications after arrest as well as diagnosis and treatment of underlying conditions that led to the cardiopulmonary arrest.
In an effort to have the entire veterinary team prepared for CPR on any animal, RECOVER guidelines recommend standardization and regular audit of resuscitation equipment as well as immediate availability of cognitive aids and descriptive CPR algorithms (eg, dose charts, checklists), which are available through the RECOVER website. Cognitive skill training and didactics should be incorporated for all veterinary team members on a regular basis. Assigning a leader and having specific leadership training, including debriefing after any CPR efforts, are recommended as well. Each team member should be familiar with available medical equipment and his or her role during CPR.
When CPA is recognized, CPR efforts should begin immediately. Early recognition and intervention is essential. Palpation of pulses is not recommended before initiating compressions, because this will delay intervention. Mouth-to-nose resuscitation should be performed until endotracheal intubation and positive-pressure ventilation with 100% oxygen can be accomplished. The compression to ventilation ratio should be 30:2. Once the airway is established, it is imperative to confirm placement with thoracic auscultation, visualization, palpation, and ETCO2 monitoring, as well as to secure the tube with a tie-in. Ventilations should be provided at a rate of 10 breaths/min, with a volume of 10 mL/kg and an inspiratory time of 1 sec. Ideally, these breaths are provided with a portable bag-valve-mask apparatus.
Simultaneous with ventilation, circulation should be promoted in small animals by compressing the chest externally. Compressions should be performed with the animal in lateral recumbency (or dorsal recumbency for barrel-chested animals, such as Bulldogs). Compressions should be performed over the widest part of the thorax using the "thoracic pump" technique. In keel-shaped animals (such as Greyhounds or cats), compressions may be performed directly over the heart (at the fourth and fifth intercostal space) using the "cardiac pump" technique. The compression rate should be 100–120 compressions/min regardless of size. Each compression should be delivered quickly in a cough-like fashion and should compress the chest wall ⅓ to ½ of the width and allow full recoil of the chest. When the cardiac pump technique is used, direct compression of the ventricles of the heart contribute to forward blood flow; in the thoracic pump technique, changes in thoracic pressure are the important mechanism to generate forward blood flow. Simultaneous ventilations and compressions should be done in 2-min cycles; individuals performing the ventilation and compressions should change functions every 2 min to prevent fatigue and less-effective compressions. Interruptions to chest compressions to assess ECG or auscult the heart should be minimal. Interposed abdominal compressions may be added for animals without abdominal disease if adequately trained staff is available. This is performed by placing both hands on the abdomen and compressing quickly, timing the compression to be done between chest compressions.
The goal is to improve venous return to the heart during the diastolic phase of the compression cycle. Monitoring CPR (see below) may necessitate a change in CPR technique.
In ACLS, an ECG is obtained to characterize arrhythmias, followed by drug administration or defibrillation as indicated. The purpose is to reestablish electrical and mechanical activity of the heart. The major arresting rhythms in veterinary medicine include sinus bradycardia, asystole, pulseless electrical activity (PEA, previously termed electromechanical dissociation), and ventricular fibrillation or flutter. Drugs are selected based on the arrhythmia or known/suspected underlying disease and can be administered by intravenous, intraosseous, or intratracheal routes (see Table: Drugs and Defibrillation Used in Cardiopulmonary Resuscitation). Drugs that can be administered intratracheally include naloxone, atropine, vasopressin, epinephrine, and lidocaine (best remembered by the acronym NAVEL); the dosage for all drugs is usually doubled when administration is intratracheal. Intracardiac administration of drugs is no longer recommended, because arrhythmias, myocardial hemorrhage, and myocardial vessel laceration may occur.
Drugs and Defibrillation Used in Cardiopulmonary Resuscitation
If the animal is known or suspected to be hypovolemic, isotonic balanced crystalloid solutions should be rapidly infused to restore volume and promote perfusion. Synthetic colloids such as hetastarch, hydroxyethyl starch, dextran 70, or stroma-free hemoglobin rapidly expand the intravascular volume with much smaller infusion volumes required. Overzealous fluid administration can result in fulminant pulmonary edema due to poor myocardial contractility and arrhythmias. Fluids should not be administered to euvolemic animals, because the increase in central venous pressure may reduce myocardial and cerebral blood flow. Metabolic alterations such as hyperkalemia, hypocalcemia, and severe acidosis should be treated when evident but not otherwise.
Impedance threshold devices may be considered an adjuvant to therapy and used only on animals weighing >10 kg.
If closed chest BCLS is unsuccessful (as determined by lack of spontaneous respiration or inability to generate detectable forward blood flow) after 5–10 min, open-chest CPR (see below) is indicated. Instances when open-chest CPR is indicated during initial BCLS include unwitnessed arrest, recent abdominal or thoracic surgery, suspected pleural or pericardial disease, trauma or pathology of the chest or abdominal wall with blood loss, diaphragmatic hernia, and in larger dogs in which external compressions are unlikely to generate an adequate forward blood flow.
Asystole appears as a flat line on the ECG and suggests complete absence of electrical activity. In arrest situations known or suspected to be associated with hyperkalemia, calcium gluconate should be administered. Regular insulin at 0.2 U/kg, followed by glucose at 1–2 g/U of insulin, diluted to 25%, temporarily reduces serum levels of potassium. Epinephrine or vasopressin, with or without atropine can be administered in an attempt to generate impulses. Fine ventricular fibrillation may look like asystole, and for this reason, open-chest heart massage and direct observation of myocardial activity are warranted early with this arrhythmia; if fibrillation is visualized, defibrillation is indicated.
This rhythm implies that multiple foci within the ventricles are firing rapidly and independently, resulting in no coordinated mechanical activity. There are no ventricular contractions and no cardiac output. The goal is to abruptly stop the electrical activity and allow one strong (hopefully normal) electrical rhythm to take over. Defibrillation is more successful when there are few, strong foci (coarse fibrillation) than when there are multiple, weak foci (fine fibrillation).
The ECG tracing can be normal or show an arrhythmia (commonly a bradyarrhythmia of ventricular or supraventricular origin), but the heart has no muscular activity associated with the electrical activity, ie, no contractions and no cardiac output and, subsequently, no pulses. In this arrhythmia, it is vital that thoracic auscultation be performed in tandem with central pulse (femoral arterial) palpation and ECG evaluation. There are no heart sounds or pulse activity. However, severe hypovolemia, pericardial effusion, and significant accumulation of fluid or air in the pleural cavity can prevent detection of normal heart sounds. The ECG associated with these conditions demonstrates tachyarrhythmias, in contrast to the usually normal or slow rate of PEA. Atropine and epinephrine or vasopressin may be given in an attempt to correct this arrhythmia. Defibrillation may be attempted with pulseless ventricular tachycardia.
Sinus bradycardia on the ECG has P, QRS, and T waves that appear normal, except they occur at a much slower rate. This arresting rhythm may be caused by many disease processes, such as high vagal tone due to GI, urinary, or thoracic disease, and hyperkalemia due to urinary obstruction or rupture and prolonged CPA with CPR efforts. Treatment of known or suspected hyperkalemia with calcium gluconate, insulin, and dextrose with or without sodium bicarbonate may be necessary. Atropine is indicated in this arrhythmia.
If the CPA is believed to be associated with drug administration, a reversal agent should be administered in addition to treating arrhythmias in ACLS. Benzodiazepines such as diazepam and midazolam are reversed with flumazenil, opioid medications such as fentanyl and morphine-related drugs can be reversed with naloxone or partially reversed with butorphanol, xylazine can be reversed with yohimbine, and dexmedetomidine can be reversed with atipamezole. If inhalant anesthesia was used, it should be discontinued and the anesthetic circuit flushed with fresh oxygen.
If possible, a quick clip of the hair along the intended incision site is helpful. Usually, there is no time for a full aseptic preparation of the area. A scalpel blade or Mayo scissors are used to incise the skin and subcutaneous tissues along the cranial border of the fourth or fifth rib from the spine to sternum. A Carmalt forceps or Mayo scissors are used to bluntly dissect through the underlying muscle tissues and push through the pleura. Ventilations should be discontinued momentarily, and the instrument should be guarded with a thumb and forefinger as the pleura is entered to prevent injury to the heart or lungs. After the pleura is entered at the ventral aspect of the incision, Mayo scissors are used to incise the muscles dorsally along the entire length of the intercostal space, along the cranial aspect of the rib. Care should be taken to avoid incising the internal thoracic vessels running parallel and lateral to the sternum. After the chest cavity is opened, manual ventilations should continue, and the pericardiodiaphragmatic ligament elevated and incised with scissors, extending the incision dorsally to just ventral to the phrenic nerve. The heart is then lifted out of the pericardial sac and observed for any coordinated spontaneous contractions. If no cardiac contractions are noted, the heart is grasped with one or both hands and compressed progressively from the apex to the base. The compression is then released to allow the cardiac chambers to refill with blood. If fine or coarse fibrillation of the heart muscle is noted, internal defibrillation should be performed.
The descending aorta can be isolated and temporarily cross-clamped to direct blood flow to the brain. Aortic cross-clamping can be performed with atraumatic vascular clamps or by using a modified Rommell tourniquet, passing a rubber tube, latex tube, or umbilical tape around the aorta with the assistance of curved hemostats and then clamping on the tube to occlude aortic flow. Aortic cross-clamping can be performed for 10 min without serious complications (from lack of blood flow to the spinal cord).
An ECG is evaluated and drugs given as indicated during ACLS procedures. Return of spontaneous circulation allows lavage of the thorax with large quantities of sterile, warm, isotonic saline; placement of a thoracostomy tube; and surgical closure of the thorax. Cardiovascular support (see Circulation) is frequently required to maintain circulation while the underlying cause of the arrest is treated.
End-tidal CO2 (ETCO2) should be measured in intubated patients at risk of having CPR and is a useful monitoring tool during CPR efforts. Using an ETCO2 reading along with visualization, palpation, and auscultation can help confirm endotracheal intubation. ETCO2 may also be an early indicator of return of spontaneous circulation (ROSC) and effectiveness of CPR efforts (when minute ventilation is consistent). An ETCO2 of <10 mmHg indicates esophageal intubation, ineffective CPR technique, incorrect placement of endotracheal tube, or hyperventilation (if adequate perfusion is established). An ETCO2 reading of 12–18 mmHg indicates an ROSC, and a reading of >45 mmHg may indicate hypoventilation or increased CO2 delivery to the lungs after ROSC occurs.
Routine monitoring of ECG is essential during CPR to allow identification and specific therapy of arrhythmias. Palpation of pulses either to detect CPA or to monitor effectiveness of CPR efforts is not recommended because of the insensitive nature of this test. Use of Doppler monitoring (on eyes or peripheral arteries) to detect CPA or monitor efforts of CPR is also not recommended.
Use of blood samples may help guide therapy in some instances during CPR. Centrally collected samples are ideal; however, most patients do not have a central catheter. Peripheral blood samples do not necessarily reflect the central circulation but may help guide therapy in some instances (such as hyperkalemia). It is not recommended to monitor with arterial gas samples or pulse oximetry; these require pulsatile arterial flow, which is inadequate during CPR.
Close monitoring of an animal after arrest is vital, because significant abnormalities of acid-base and electrolytes (especially hyperkalemia) are common and may require additional treatment. Parameters such as ECG, blood pressure, neurologic status, pulse oximetry, ETCO2, and venous blood gases should be monitored closely. Blood pressure support with dopamine, dobutamine, other pressor agents, or stroma-free hemoglobin, as indicated, may be required to maintain cardiac output. Body temperature, glucose, and lactate may provide additional information.
With anaerobic metabolism that occurs during shock and cardiopulmonary arrest, blood lactate levels (see Electrolytes and Acid-Base Balance) rise dramatically (normal levels are <2 mmol/L). With ROSC, lactate levels may rise dramatically and then resolve with appropriate treatment.
Routine use of large volumes of fluids is not recommended and should be avoided in animals with congestive heart failure. It is important to use resuscitation endpoints during post-CPA care to normalize venous oxygen content, lactate, blood pressure, central venous pressure, PCV, and oxygen saturation. Medications to help reduce cerebral edema, such as mannitol and furosemide, can be administered after CPA and are often recommended to help decrease cerebral edema. Routine mechanical ventilation is not routinely recommended but reasonable in animals that are hypercapneic or hypoxemic. Vasopressors and positive inotropes are reasonable when needed. Animals with open-chest CPR will require control of hemorrhage, pleural lavage, placement of a chest tube, perioperative antibiotics, and closure of the thoracic cavity. A large percentage of animals that sustain a CPA will have another episode of CPA. Treatment of the underlying condition that led to the CPA is essential to help prevent recurrence.