The success of cardiopulmonary-cerebral resuscitation (CPCR) efforts depends on the underlying cause of the arrest and on the timeliness and effectiveness of the intervention. CPCR is divided into 3 stages: 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; and post-resuscitation management, which involves intensive monitoring of common post-arrest complications as well as diagnosis and treatment of underlying conditions that led to the cardiopulmonary arrest.

Basic Cardiac Life Support

Mouth-to-nose resuscitation should be performed until endotracheal intubation and positive-pressure ventilation with 100% oxygen can be accomplished. Once the airway is established with endotracheal intubation, 2 quick breaths are given while the chest is auscultated to confirm endotracheal tube placement, and the tube is secured with a tie-in. Ventilations should be provided at 20–40 breaths/min. End-tidal CO₂ can be monitored during CPCR efforts. A reading of <10 mm Hg indicates esophageal intubation, ineffective CPCR technique, or hyperventilation (if adequate perfusion is established). An end-tidal CO₂ reading of 12–18 mm Hg indicates a return of spontaneous circulation, and a reading of >45 mm Hg may indicate hypoventilation or increased CO₂ delivery to the lungs after successful resuscitation.

Circulation should be promoted in small animals by compressing the chest externally over the area of the heart, generally over the fourth and fifth intercostal space, while the animal is in lateral recumbency (cardiac pump technique). Dogs weighing >15 kg can be placed in right lateral recumbency and chest compressions applied over the widest part of the chest (thoracic pump technique). Alternatively, larger dogs can be placed in dorsal recumbency with chest compressions applied over the caudal one-third of the sternum. The compression rate should be 80–120/min. Each compression should be delivered quickly in a cough-like fashion and should compress the chest wall ~30%. In dogs weighing <15 kg, the direct compression of the heart may contribute to forward blood flow, but the change in pressure that occurs in the thorax as a whole is considered to be the more important mechanism for generating forward flow. Compressions should be discontinued only for a rapid reassessment of the patient with auscultation, palpation, and examination of the ECG.

Perfusion should be quickly assessed to determine the effectiveness of basic life-support procedures by using a Doppler probe on the eye or end-tidal CO₂ measurement. If perfusion is inadequate, procedures should be modified as necessary. Abdominal counterpressure can be initiated if there is no intra-abdominal pathology. Abdominal counterpressure is performed by placing both hands on the ventral surface of the abdomen and thrusting quickly in a dorsal direction, timing the abdominal compression to occur between chest compressions. The goal is to improve venous return to the heart during the diastolic phase of the compression cycle. Abdominal counterpressure is contraindicated in animals with known or suspected trauma and recent abdominal surgery.

Advanced Cardiac Life Support

In ACLS, an ECG is obtained to characterize arrhythmias, followed by drug administration or defibrillation as indicated. The purpose is to reestablish electrical and myocardial 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 and can be administered by intravenous, intraosseous, or intratracheal routes (see Specific Diagnostics and Therapy: Drugs Used in Cardiopulmonary-Cerebral Resuscitation, Dosages, and Indications). 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 given intratracheally. Intracardiac administration of drugs is no longer recommended because arrhythmias, myocardial hemorrhage, and myocardial vessel laceration may occur.

Table 1
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Drugs Used in Cardiopulmonary-Cerebral Resuscitation, Dosages, and Indications Drug Dosagea Indications Epinephrine 1 mL/5–10 lb (1:10,000 concentration) Asystole, ventricular fibrillation, PEAb Atropine 0.1 mL/5 lb (0.5 mg/mL solution) Sinus bradycardia, asystole, PEA Sodium bicarbonate 0.2–2.0 mL/kg (1 mEq/mL solution) Severe metabolic acidemia associated with prolonged cardiopulmonary resuscitation efforts (must adequately ventilate to be effective), hyperkalemia Calcium gluconate 1 mL/5–10 kg (2% solution without epinephrine) PEA, pulseless idioventricular rhythm, hyperkalemia Amiodarone 5 mg/kg Ventricular fibrillation or pulseless ventricular tachycardia Magnesium sulfate 30 mg/kg Hypomagnesemia, torsades de pointes Lidocaine 2–4 mg/kg Ventricular flutter, ventricular fine fibrillation Vasopressin 0.4–0.8 U/kg Asystole, bradycardia, PEA a Dosage should be doubled if given via intratracheal or sublingual route. b PEA = pulseless electrical activity

If the patient is known or suspected to be hypovolemic, isotonic balanced electrolyte crystalloid solutions should be rapidly infused to restore volume and promote perfusion. Synthetic colloids such as hetastarch, dextran 70, or stroma-free hemoglobin rapidly expand the intravascular volume with a much smaller volume required. Over-zealous fluid administration can result in fulminant pulmonary edema due to poor myocardial contractility and arrhythmias. Fluids should be administered with caution in euvolemic animals because the increase in central venous pressure may reduce myocardial and cerebral blood flow.

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 CPCR (see Specific Diagnostics and Therapy: Open-Chest Cardiopulmonary Resuscitation) is indicated. Instances when open-chest CPCR is indicated during initial BCLS include unwitnessed arrest, recent abdominal or thoracic surgery, suspected pleural or pericardial disease, trauma to 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.

Arrhythmias of Cardiac Arrest

Asystole

Asystole appears as a flat line on the ECG and suggests complete absence of electrical activity. Animals in asystole can be assumed to have hyperkalemia until proved otherwise. 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 temporarily reduces serum levels of potassium. Atropine and epinephrine can be administered in an attempt to generate impulses. Many arrhythmias that appear to be asystole are, in fact, fine ventricular fibrillation. For this reason, open-chest heart massage and direct observation of myocardial activity are warranted early with this arrhythmia. Administration of epinephrine and defibrillation may be indicated.

Ventricular Flutter

This rhythm is more chaotic than ventricular tachycardia and is prefibrillatory. Lidocaine is the drug of choice to block the excited focus. If lidocaine is ineffective after 2 boluses and perfusion is absent, defibrillation may be required.

Ventricular Fibrillation

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 focus to take over. Defibrillation is more successful when there are few, strong foci (coarse fibrillation) than when there are multiple, weak foci (fine fibrillation).

Pulseless Electrical Activity (PEA)

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. 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 heart sounds in a beating heart. The ECG associated with these conditions demonstrates tachyarrhythmias, in contrast to the usually normal or slow rate of PEA. PEA has a grave prognosis. 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

Sinus bradycardia on the ECG has P, QRS, and T waves that appear normal, but they occur at a much slower than normal 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 CPCR efforts. Treatment of known or suspected hyperkalemia with calcium gluconate, insulin, and dextrose may be necessary. Atropine is indicated in this arrythmia.

If the cardiopulmonary arrest 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.

Open-Chest Cardiopulmonary Resuscitation

(Emergency thoracotomy)

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; Mayo scissors may be used for this as well. 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, rubber shod clamps, Forrester sponge forceps, or by passing a rubber tube, latex tube, or umbilical tape around the aorta and tightening by sliding a hemostat down just above the aorta. Aortic cross-clamping can be performed for 10 min without serious complications.

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 chest tube; and surgical closure of the thorax. Cardiovascular support (see Evaluation and Initial Treatment of the Emergency Patient: Circulation) is frequently required to maintain circulation while the underlying cause of the arrest is treated. Close monitoring of a post-arrest patient 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, and pulse oximetry also should be monitored closely. Blood pressure support with dopamine, dobutamine, or stroma-free hemoglobin, as indicated, may be required to maintain cardiac output.

With anaerobic metabolism that occurs during shock and cardiopulmonary arrest, blood lactate levels (see Monitoring Procedures for the Critically Ill Animal: Electrolytes and Acid-Base Balance) rise dramatically (normal levels are <2 mmol/L). With return of spontaneous circulation, lactate levels may rise dramatically and then resolve with appropriate treatment. Medications to help reduce cerebral edema, such as mannitol and furosemide, can be administered after a cardiopulmonary arrest.

Last full review/revision March 2012 by Rebecca Kirby, DVM, DACVIM, DACVECC; Andrew Linklater, DVM, DACVECC