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Veterinarian Technician April 2011 (Vol 32, No 4)

Managing Cardiopulmonary Arrest

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

    CETEST This course is approved for 1.0 CE credits

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    Cardiopulmonary arrest (CPA) is characterized by abrupt, complete failure of the respiratory and circulatory systems. The lack of cardiac output and oxygen delivery to tissues (DO2) can quickly cause unconsciousness and systemic cellular death from oxygen starvation. If left untreated, cerebral hypoxia results in complete biologic brain death within 4 to 6 minutes of CPA.1,2 Therefore, prompt cardiopulmonary cerebral resuscitation (CPCR) is imperative. Veterinary technicians can play a key role in ensuring that patients receive this treatment.

    Causes and Clinical Signs

    In dogs and cats, common causes of CPA include anesthetic complications; vagal stimulation; hypovolemia; severe trauma, such as 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 (e.g., agonal breathing, decreased rate, sudden increased rate); the absence of a pulse; significant hypotension (i.e., systolic blood pressure <50 mm Hg [normal: >90 to 100 mm Hg]); irregular or inaudible heart sounds; changes in the heart rate or rhythm; change in mucous membrane color (e.g., white or cyanotic); fixed, dilated pupils; distressed vocalizations; and 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 because patients in arrest are nonresponsive and apneic, with no detectable pulse.


    Hemothorax—accumulation of blood in the pleural cavity

    Hyperkalemia—an abnormally high concentration of potassium ions in the blood

    Hypovolemia—a decreased blood volume

    Hypoxia—deficiency in the amount of oxygen reaching the body tissues

    Pneumothorax—accumulation of air or gas in the pleural cavity

    Thoracentesis—removal of fluid or air from the chest through a needle or tube

    Transcutaneous pacing (also called external pacing)—a temporary means of pacing a patient’s heart by delivering pulses of electric current through the patient’s chest, which stimulates contraction of the heart

    Cardiopulmonary Cerebral Resuscitation

    CPCR is initiated in three stages: basic life support (BLS), advanced life support (ALS), and postresuscitative care.3 Adopted from human emergency medicine, BLS 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. ALS includes advanced care such as establishing 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 a veterinarian, may be necessary if the airway obstruction is not immediately resolved. Insertion of a large-gauge 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. In some cases, material fully obstructing the airway (e.g., a ball) can be manually removed with long hemostats or Doyen intestinal clamps.

    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 should then 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 Therefore, choosing a lower rate from the range of 10 to 24 breaths/min may be advised; these rates may be reexamined in future literature.

    Veterinary patients can be easily and safely ventilated with an Ambu bag (FIGURE 1) or 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 <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 performed by a veterinarian may be necessary.

    Acupuncture has also been used to help treat CPA and respiratory depression.7 Needling the acupuncture point GV26 can help stimulate respiration and increase cerebral oxygen.8–10 This acupoint can be stimulated by inserting a regular 25-gauge needle or acupuncture needle into the nasal philtrum to a depth of approximately 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 detectable heartbeat. External cardiac massage at a rate of 80 to 120 compressions/min is recommended,6 but higher rates within that range seem to work better.11 Small patients (<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 pliable chest walls. Closed-chest compressions in large patients, however, generally are inadequate in compressing the ventricles. Therefore, the thoracic pump theory, which suggests that forward blood flow in larger patients is the result of a generalized increase in intrathoracic pressure, is used in these patients. 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.12–14

    Based on the “2010 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”15and the “2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Care Science With Treatment Recommendations,”16 rescuers performing chest compressions should push hard and fast, allow full chest recoilafter each compression, and minimize interruptions in compressions.It is critical for chest compressions to be continuous after they have begun.

    Guidelines for open-chest internal cardiac massage (ICM), which is performed by a veterinarian, typically recommend its immediate use in all patients >40 lb (18 kg); in patients after 10 minutes of unsuccessful CPCR, regardless of their size; and in all cases of trauma and/or hemorrhage, such as patients with pneumothorax, hemothorax, or cardiac tamponade.5,17 ICM allows direct visualization of the heart, aortic compression or temporary ligation, and internal defibrillation. In addition, ICM can increase cardiac output, blood pressure, coronary perfusion pressure, and cerebral perfusion pressure compared with closed-chest CPCR and has been associated with increased return of spontaneous circulation and improved neurologic outcomes in animal models.11,18

    BOX 1. Impedance Threshold Devices

    The development of impedance threshold devices (ITDs) has shown promise in both human and animal models.19 The ITD is a small, inexpensive device that is placed on the proximal end of an endotracheal tube during resuscitation to create an increase in negative pressure during the chest-recoil phase of chest compression. An increase in negative pressure creates a vacuum that results in more blood being pulled into the heart and, therefore, more blood output during the next compression. ITDs include a timing light that helps the rescuer ventilate the patient at the proper rate to avoid hyperventilation.
    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; however, compressions should never be stopped for an assessment. With sufficient water-based lubricant, a Doppler transducer can be placed directly over one of the patient's open eyes. 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 (BOX 119) or ICM should be considered.

    CPCR Stage 2: Advanced Life Support

    Establishing venous access is important but shouldnever interfere with chest compressions or defibrillation.Venous access can be established by using methods such as intraosseous catheter placement and venous cutdown, in which a small opening is created in the skin to allow passage of a needle or cannula into a vein. The jugular vein typically yields well to catheterization during CPA and provides the shortest transit time for drugs to reach the heart.20 After venous access has been established, aggressive fluid administration should be considered if hypovolemia existed before the CPA 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 administration of hypertonic saline, crystalloids, colloids, blood products, and hemoglobin-based oxygen-carrying solutions.20

    If an IV catheter cannot be placed initially, emergency drugs (e.g., lidocaine, epinephrine, atropine, vasopressin, naloxone) can be administered through an endotracheal tube.20 Typically, a long red rubber catheter is inserted down the tube, and drugs are administered through the catheter. Drug doses administered this way 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.21

    Intracardiac injection of medication is contraindicated, especially during closed-chest CPCR. Inaccurate injection and complications, such as vessel laceration and hemorrhage, are common.22,23

    Accurate ECG interpretation, which determines the specific arrhythmia the patient is experiencing (BOX 2 20–28 FIGURE A; FIGURE B; FIGURE C) , 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, if possible.

    Unfortunately, most patients in CPA cannot be resuscitated even if CPCR is performed perfectly. End-tidal carbon dioxide measurements >15 mm Hg are reportedly associated with higher survival rates.29 Other types of arrhythmia can usually 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 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.30 Inducing mild hypothermia in patients 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 CPA.31

    Poor perfusion during CPA may also precipitate brain injury, disseminated intravascular coagulation, gut reperfusion syndrome, and renal failure. Therefore, intensive monitoring and aggressive supportive care are required to optimize management of blood pressure, cardiac output, oxygenation, ventilation, and vital organ perfusion.30,31


    After CPA, the success rate for recovery of veterinary patients is generally poor.32–34 A 1-week survival rate of <4% has been reported for cats and dogs that received CPCR following full arrest.31 However, functional recovery has been reported in most animals that survive CPA.35

    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.24,27,28

    Downloadable PDF

    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. Davies A, Janse J, Reynolds GW. Acupuncture in the relief of respiratory arrest. N Z Vet J 1984;32:109-110.

    11. 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.

    12. 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.

    13. Babbs CF. Interposed abdominal compression CPR: a comprehensive evidence-based review. Resuscitation 2003;59(1):71-82.

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

    15. Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122(suppl 3):S640-S656.

    16. Hazinski MF, Nolan JP, Billi JE, et al. 2010 international consensus on cardiopulmonary resuscitation and emergency care science with treatment recommendations. Resuscitation 2010;81(1; suppl 1):e1–e332.

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

    18. 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.

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

    20. 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.

    21. 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.

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

    23. 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.

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

    25. Schmittinger CA, Astner S, Astner L, et al. Cardiopulmonary resuscitation with vasopressin in a dog. Vet Anaesth Analg2005;32(2):112-114.

    26. Bright JM, Wright BD. Successful biphasic transthoracic defibrillation of a dog with prolonged refractory ventricular fibrillation. J Vet Emerg Crit Care 2009;193:275-279.

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

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

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

    30. 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.

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

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

    33. Wingfield WE, van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA1992;200(12):1993-1996.

    34. 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.

    35. 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 »

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