Welcome to the all-new Vetlearn

  • Vetlearn is becoming part of NAVC VetFolio.
    Starting in January 2015, Compendium and
    Veterinary Technician articles will be available on
    NAVC VetFolio. VetFolio subscribers will have
    access to not only the journals, but also:
  • Over 500 hours of CE
  • Community forums to discuss tough cases
    and networking with your peers
  • Three years of select NAVC Conference
  • Free webinars for the entire healthcare team

To access Vetlearn, you must first sign in or register.


  Sign up now for:
Become a Member

Veterinarian Technician November 2008 (Vol 29, No 11)

Management of Cardiopulmonary Arrest

by Christopher Norkus, BS, CVT, VTS (ECC), VTS (Anesthesia)

    CETEST This course is approved for 0.5 CE credits

    Start Test

    Cardiopulmonary arrest (CPA) is characterized by abrupt, complete failure of the respiratory and circulatory systems. The lack of successful oxygen transport can quickly cause unconsciousness and systemic cellular death from oxygen starvation. If left untreated, cerebral hypoxia results in complete biological brain death within 4 to 6 minutes of a CPA event.1,2Therefore, prompt cardiopulmonary cerebral resuscitation (CPCR) is imperative. Veterinary technicians play a key role in ensuring that patients receive this treatment within that period.

    Causes, Clinical Signs, and Staging

    In dogs and cats, common causes of CPA include anesthetic complications; vagal stimulation; severe trauma, such as hypovolemia or pneumothorax; unstable cardiac arrhythmias, such as unstable ventricular tachycardia; severe electrolyte disturbances, such as hyperkalemia; cardiorespiratory disorders, such as congestive heart failure, hypoxia, or pericardial tamponade; and debilitating or end-stage diseases, such as sepsis or cancer.

    Potential signs of impending CPA include dramatic changes in breathing effort, rate, or rhythm; the absence of pulse; significant hypotension, with a systolic blood pressure reading of less than 50 mm Hg; irregular or inaudible heart sounds; changes in the heart rate or rhythm; changes in the mucous membrane color; fixed, dilated pupils; and patient collapse.

    Assessment of the patient is crucial if CPA is suspected. Before CPCR is initiated, it is essential to evaluate the patient's responsiveness, breathing pattern, and pulse, as patients in arrest will be nonresponsive and apneic, with no detectable pulse.

    CPCR is initiated in three stages: basic life support (BLS), advanced life support (ALS), and postresuscitative care.3 Adopted from human emergency medicine, the BLS stage involves establishing an open and clear airway, providing assisted ventilation, and performing chest compressions. These steps are often called the ABCs — airway, breathing, and circulation. The ALS stage includes such advanced care as venous access, interpretation of an electrocardiogram (ECG), drug administration, and defibrillation and is typically performed by credentialed veterinary technicians, veterinarians, or both. Postresuscitative care includes intensive monitoring as well as cardiovascular and ventilatory support.

    CPCR Stage 1: Basic Life Support

    Airway management involves extending the patient's neck to straighten the airway and pulling the patient's tongue forward. The veterinary staff should quickly examine the upper airway and initiate suctioning, if necessary. All foreign material or vomit observed in the patient's mouth should be cleared immediately.

    If the patient's airway is fully obstructed, abdominal thrusts and finger sweeps of the pharynx can help dislodge the obstruction. An emergency tracheotomy, which is performed by the veterinarian, may be necessary if the airway obstruction is not immediately resolved. Insertion of a needle or intravenous (IV) catheter directly into the trachea below the obstruction, along with oxygen administration, can be useful while the tracheotomy is being performed.

    After the patient's airway has been cleared, an endotracheal tube should be placed. Tube placement should be confirmed and the tube secured and cuffed. The patient then should be ventilated with 100% oxygen.

    Proper ventilation is a critical component of BLS. Based on the most recent published recommendations, veterinary patients should receive 100% oxygen at a rate of 10 to 24 breaths/min.4,5 In humans, more frequent ventilation has been shown to be significantly detrimental because it can result in decreased myocardial and cerebral perfusion.6

    Veterinary patients can be easily and safely ventilated with a bag-valve mask. Using an anesthesia unit can be slow and ineffective because the pop-off valve must be opened and closed repeatedly. Peak airway pressure should be less than 20 cm H2O.4 Lack of chest wall motion, poor ventilation, or absence of lung sounds should prompt an immediate search for a poorly positioned tube or a severe pleural space disorder, such as pneumothorax. In these cases, thoracentesis or thoracotomy, which is performed by the veterinarian, may be necessary.

    Acupuncture also has been used to treat CPA and arrhythmias.7 Needling the acupuncture point GV26 can help stimulate respiration and increase cerebral oxygen.8,9 This point can be stimulated by inserting a regular 25-gauge needle or acupuncture needle into the nasal philtrum to a depth of about 10 to 20 mm and performing jabs in a hen-pecking motion while monitoring for improvement in respiration.8

    The goal of circulatory support during CPCR is to maximize myocardial and cerebral perfusion. Chest compressions should be performed immediately in patients without a pulse. External cardiac massage (ECM) at a rate of 80 to 120 compressions/min is recommended,6 but higher rates within that range seem to work better.10 Small patients weighing less than 15 lb (7 kg) should receive compressions directly over the heart (cardiac pump theory), whereas larger patients should receive more caudal compressions that are directed over the widest part of the chest (thoracic pump theory).

    The cardiac pump theory asserts that arterial blood flow is a result of direct compression of the ventricles and, therefore, makes sense in small patients with compliable chest walls. Closed-chest compressions in large patients, however, generally are inadequate in actually compressing the ventricles. Therefore, the thoracic pump theory is used and suggests that forward blood flow in larger patients is actually the result of a generalized increase in intrathoracic pressure. Ideally, two technicians should perform interposed abdominal compressions, in which alternate compressions of the cranial abdomen and the chest are completed at a rate of 70 to 90 compressions/min. This has been shown to increase cardiac output.11,12

    Guidelines for open-chest internal cardiac massage (ICM) typically recommend its immediate use in all patients weighing more than 40 lb (18 kg), in patients after 10 minutes of CPCR regardless of their size, and in all cases of trauma and/or hemorrhage, such as patients with pneumothorax, hemothorax, or cardiac tamponade.5,13 ICM allows direct visualization of the heart, aortic compression or cross-clamping, and internal defibrillation. ICM also can increase cardiac output, blood pressure, coronary perfusion pressure, and cerebral perfusion pressure compared with closed-chest CPCR and has been associated with the increased return of spontaneous circulation and improved neurologic outcomes in animal models.10,14

    The veterinary staff should regularly assess the effectiveness of CPCR by palpating for the presence of pulses during compressions and by using a Doppler ultrasound transducer. With sufficient water-based lubricant, a Doppler transducer can be placed directly over one of the patient's open eyeballs. The presence of a "swooshing" wave sound from the Doppler unit during concurrent chest compressions can provide a crude estimate of whether forward blood flow is reaching the brain. If chest compressions are not generating adequate forward blood flow, either the patient should be repositioned and the resuscitation technique changed to increase intrathoracic pressure or ICM should be considered.

    CPCR Stage 2: Advanced Life Support

    Venous access can be established by using such methods as intraosseus catheter placement and venous cutdown, in which a small opening is created in a vein to allow passage of a needle or cannula. The jugular vein typically yields well to catheterization during CPA and provides the shortest transit time for drugs to reach the heart.16 After venous access has been established, aggressive fluid administration should be considered if hypovolemia existed before the CPA event or if the patient is experiencing blood loss. However, overzealous fluid administration in patients with normal body fluid volume may be detrimental. Fluid resuscitation can include hypertonic saline, crystalloids, colloids, blood products, and hemoglobin-based oxygen-carrying solutions.16

    If an IV catheter cannot be placed initially, emergency drugs, such as lidocaine, epinephrine, atropine, and naloxone, can be administered through the endotracheal tube.16 Typically, a long red rubber catheter is inserted down the tube, and drugs are administered through the catheter. Drug doses are normally increased two- to threefold and are followed by a small saline chaser to ensure successful drug passage into the lungs. For example, the dose for IV atropine is 0.02 mg/kg, but if it is administered through the endotracheal tube, the dose would be 0.04 to 0.06 mg/kg.17

    Intracardiac injection of medication is contraindicated, especially during closed-chest CPCR. Inaccurate injection and complications, such as vessel laceration and hemorrhage, are common.18,19

    Accurate ECG interpretation, which determines the specific arrhythmia the patient is experiencing (see Treating Arrhythmias ), is necessary before CPA can be treated. After the type of arrhythmia has been established, drug administration and defibrillation can be initiated. If CPA occurs as a result of anesthesia, all anesthetic agents must be immediately discontinued and their effects reversed.

    Unfortunately, most patients in CPA cannot be resuscitated even if CPCR is performed perfectly. End-tidal carbon dioxide measurements higher than 15 mm Hg are reportedly associated with higher survival rates.24 Some have suggested that arrhythmias, such as asystole, not be treated for more than 5 minutes or with more than two rounds of epinephrine, although there are no published studies confirming that premise. Other types of arrhythmia usually can be treated until they progress to asystole, unless the patient's owner declines further resuscitation efforts.

    CPCR Stage 3: Postresuscitative Care

    Patients that are restored to a perfusing cardiac rhythm commonly experience rearrest — often within minutes to several hours — especially if the original cause of the CPA event has not been identified. Therefore, resuscitated patients usually require substantial cardiovascular and ventilatory support during the period following CPA. Mild hypothermia after resuscitation from CPA decreases cerebral oxygen demand and has been shown to improve outcomes in dogs.25 Inducing mild hypothermia in the patient could be considered a therapeutic option. In human patients, hyperglycemia has been shown to be associated with worse neurologic outcomes and should, therefore, be avoided after a CPA event.26

    The poor perfusion state present during CPA also may precipitate brain injury, disseminated intravascular coagulation, gut reperfusion syndrome, and renal failure. Therefore, intensive monitoring and aggressive supportive care are required to optimize blood pressure, cardiac output, oxygenation, ventilation, and vital organ perfusion.25,26

    Closing Remarks

    After CPA, the success rate for recovery of veterinary patients is generally poor.27-29 A 1-week survival rate of less than 4% for both cats and dogs that received CPCR following full arrest has been reported.27 However, functional recovery has been reported in most animals that survive CPA.30

    Based on current research, resuscitation appears to be successful in patients that are treated quickly; have a reversible underlying disease process, such as anesthetic overdose, upper airway obstruction, hemorrhage, or electrolyte abnormalities; and, ideally, are not in full CPA.20,22,23

    1. Safar P. Cerebral resuscitation after cardiac arrest: a review. Circulation 1986; 74(6 Pt 2):IV138-153.

    2. Safar P. Resuscitation from clinical death: pathophysiologic limits and therapeutic potentials. Crit Care Med 1988;16(10): 923-941.

    3. Pablo LS. Current concepts in cardiopulmonary resuscitation. World Small Anim Vet Assoc World Congr Proc:2003.

    4. Kruse-Elliott KT. Cardiopulmonary resuscitation. Strategies for maximizing success. Vet Med 2001;16(1):51-58.

    5. Henik RA. Basic life support and external cardiac compressions in dogs and cats. JAVMA 1992;200(12):1925-1931.

    6. Plunkett SJ, McMichael M. Cardiopulmonary resuscitation in small animal medicine: an update. J Vet Intern Med 2008;22(1):9-25.

    7. Schoen AM. Veterinary medical acupuncture in critical care medicine. World Small Anim Vet Assoc World Congr Proc: 2003.

    8. Looney AL. Current thoughts on cardiopulmonary arrest and resuscitation. Atlantic Coast Vet Conf Proc:2001.

    9. Janssens L, Altman S, Rogers PA. Respiratory and cardiac arrest under general anaesthesia: treatment by acupuncture of the nasal philtrum. Vet Rec 1979;105(12):273-276.

    10. Kern KB, Sanders AB, Badylak SF, et al. Long-term survival with open-chest cardiac massage after ineffective closed-chest compression in a canine preparation. Circulation 1987;75(2):498-503.

    11. Voorhees WD 3rd, Ralston SH, Babbs CF. Regional blood flow during cardiopulmonary resuscitation with abdominal counterpulsation in dogs. Am J Emerg Med 1984;2(2):123-128.

    12. Ralston SH, Babbs CF, Niebauer MJ. Cardiopulmonary resuscitation with interposed abdominal compression in dogs. Anesth Analg 1982;61(8):645-651.

    13. Barton L, Crowe DT. Open chest cardiopulmonary resuscitation. In: Bonagura JD (ed.) Kirk's Current Veterinary Therapy XIII. Philadelphia: WB Saunders; 2000:147-149.

    14. Feneley MP, Maier GW, Kern KB, et al. Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs. Circulation 1988;77(1):240-250.

    15. Yannopoulos D, Aufderheide TP. Use of the impedance threshold device (ITD). Resuscitation 2007;75(1):192-193.

    16. Emmerman CL, Pinchak AC, Hancock D, et al. Effect of injection site on circulation times during cardiac arrest. Crit Care Med 1988;16(11):1138-1141.

    17. Cole S, Otto C, Hughes D. Cardiopulmonary cerebral resuscitation in small animals — a clinical practice review. J Vet Emerg Crit Care 2003;13(1): 13-23.

    18. Sabin HI, Coghill SB, Khunti K, McNeill CO. Accuracy of intracardiac injections determined by a post-mortem study. Lancet 1983;2(8358):1054-1055.

    19. Jespersen HF, Granborg J, Hansen U, et al. Feasibility of intracardiac injection of drugs during cardiac arrest. Eur Heart J 1990;11(3):269-274.

    20. Rush JE, Wingfield WE. Recognition and frequency of dysrhythmias during cardiopulmonary arrest. JAVMA 1992; 200(12):1932-1937.

    21. Schmittinger CA, Astner S, Astner L, et al. Cardiopulmonary resuscitation with vasopressin in a dog. Vet Anaesth Analg 2005;32(2):112-114.

    22. Dani C, Bertini G, Pezzati M, et al. Brain hemodynamic effects of doxapram in preterm infants. Biol Neonate 2006; 89(2):69-74.

    23. van Pelt DR, Wingfield WE. Controversial issues in drug treatment during cardiopulmonary resuscitation. JAVMA 1992; 200:1938-1944.

    24. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration. Crit Care Med 1990;18(4):358-362.

    25. Nozari A, Safar P, Stezoski SW, et al. Mild hypothermia during prolonged cardiopulmonary cerebral resuscitation increases conscious survival in dogs. Crit Care Med 2004;32(10):2110-2116.

    26. Steingrub JS, Mundt DJ. Blood glucose and neurological outcome with global brain ischemia. Crit Care Med 1996; 24(5):802-806.

    27. Kass PH, Haskins SC. Survival following cardiopulmonary resuscitation in dogs and cats. J Vet Emerg Crit Care 1992;2(2):57-65.

    28. Wingfield WE, van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA 1992; 200(12):1993-1996.

    29. de Vos R, Koster RW, de Haan RJ, et al. In-hospital cardiopulmonary resuscitation: prearrest morbidity and outcome. Arch Intern Med 1999;159(8):845-850.

    30. Waldrop JE, Rozanski EA, Swanke ED, et al. Causes of cardiopulmonary arrest, resuscitation management, and functional outcome in dogs and cats surviving cardiopulmonary arrest. J Vet Emerg Crit Care 2004;14(1):22-29.

    References »

    NEXT: State News: Delaware

    CETEST This course is approved for 0.5 CE credits

    Start Test


    Did you know... Dogs with dilated cardiomyopathy (DCM) may show subtle clinical signs in the early stages of the disease.Read More

    These Care Guides are written to help your clients understand common conditions. They are formatted to print and give to your clients for their information.

    Stay on top of all our latest content — sign up for the Vetlearn newsletters.
    • More