Cardiopulmonary Resuscitation Lee Herold DVM, DACVECC Speaker Notes

Cardiopulmonary Resuscitation Lee Herold DVM, DACVECC Speaker Notes Cardiopulmonary arrest (CPA) is a common occurrence in the ICU and emergency veterinary practice as in human ER practice as well. In humans the international liaison committee on resuscitation (ILCOR) is a working group that has evaluated available literature on CPR to establish guidelines in human CPR. The guidelines are updated every 5 years with the most recent publication being in 2010 by the American Heart Association (AHA). ILCOR recommendations have standardized training, basic life support, and lay rescuer recommendations to improve outcomes in human CPR based on evidence based medicine. The human guidelines have been summarized and extrapolated to veterinary CPR but certain limitations were recognized in translating the AHA guidelines to veterinary species. Whereas many of the research models of cardiopulmonary arrest are performed in animals- the studies are often fibrillation studies that model the most common cardiopulmonary arrest (CPA) rhythm in humans that may not mirror what we see in dogs and cats clinically. The recommendations for catecholamine use in humans may not be able to be directly transferred to dogs and cats based on different catecholamine receptor physiology. It was also recognized that veterinary outcomes in CPR continue to lag behind those in human medicine. In several retrospective studies of veterinary CPR, there is a very wide variation of outcome in patients that underwent CPR with reports as low as 2% survival to 25% good outcome. These studies are difficult to compare directly as the outcome in these studies were not standardized. Whereas some studies state positive outcome as return of spontaneous circulation (ROSC), others use discharge from the hospital with functional neurologic recovery as a positive outcome. Irrespective of outcome measure- the success of veterinary CPR seems to be much lower than in humans with estimates of veterinary hospital discharge being <6% compared with 20% in humans. Again this may be due different functional goals in veterinary compared to human medicine. For example -it is acceptable for a human to have significant impairment or disability requiring nursing home care whereas for most of our veterinary patients- a functional dog or cat is a nearly normal dog or cat. The influence of euthanasia and cost of care may impact on veterinary success rates as well but even so there is clearly room for improvement. Recognizing these limitations the American College of Veterinary Emergency and Critical Care (ACVECC) sought to systematically review the CPR literature with the view of developing evidence based guidelines for use in dogs and cats in an effort to create a veterinary industry-wide approach to CPR. This task force was named the Reassessment Campaign on Veterinary Resuscitation (RECOVER) and culminated in the publication of the RECOVER guidelines in 2012. The RECOVER initiative based its clinical recommendations an extenstive review of the literature and devised a grading system similar to ILCOR to signify the strength behind the recommendation. Recommendations in the RECOVER initiative were given a class and followed by a level according to the table below. 2012 DoveLewis Annual Conference Page 1

Class I IIa IIb III Level A B C Recommendation Should be performed Reasonable to perform May be considered Should NOT be performed Criteria for recommendation High quality or high level of evidence studies Few to no high quality or level of evidence studies Concensus or expert opinion, standard of care, or based on physiologic principles Readiness: The importance of readiness cannot be over emphasized in veterinary CPR. The strength of these recommendations are all Class 1 recommendations and include- dedicated, regularly stocked crash carts. CPR algorithms and drug dosing charts should be readily available. Effective team communication, CPR hands on and didactic training, with refresher courses is recommended. The goal of CPR is to optimize cerebral perfusion pressures and coronary perfusion pressures. With this in mind recall that: Cerebral Perfusion Pressures=Mean Arterial Pressure- Intracranial Pressure Coronary Perfusion Pressure= Aortic diastolic pressure-right Atrial Pressure Optimization of coronary and cerebral perfusion pressures has been associated with improved outcomes in humans. The ILCOR and RECOVER guidelines converge and agree that the rapid recognition of CPA, the rapid implementation of effective cardiac compressions and administration of basic life support should be emphasized in CPR. Basic Life Support (BLS) includes obtaining a patent airway, initiating cardiac compressions (external or internal) to improve coronary and cerebral perfusion. Advanced life support (ALS) is the recognition and treatment of cardiac arrythmias, fluid therapy, defibrillation and correction of electrolyte derangements associated with CPA. The ABC pneumonic should be followed in the initiation of CPR in veterinary patients. Airway should be established with orotracheal intubation in most veterinary patients. Direct visualization with laryngoscope is essential to ensure appropriate intubation, alternatively manual palpation of epiglottis and vocal folds can be performed to ensure appropriate intubation. If severe facial trauma or upper airway obstruction precludes orotracheal intubation then rapid tracheostomy can be performed to secure an airway. Clinicians should become well versed in performing orotracheal intubation in many positions (lateral, dorsal intubation, etc) to avoid large manipulations of the patient that 2012 DoveLewis Annual Conference Page 2

may have sustained cervical or head trauma. 100% oxygen should be supplied and the patient should be ventilated at respiratory rates of 10 breathes per minute with ambu bag, an anesthetic machine can be used if ambubag is not available but the anesthetic circuit should be thoroughly flushed or a y-connector device placed on the machine that rapidly bypasses the vaporizer circuit on the anesthetic machine. Chest Compressions- There are two primary mechanisms of generating blood flow with cardiac compression- the cardiac pump and the thoracic pump mechanism. It is likely that both mechanisms operate in the majority of patients; however, the cardiac pump technique is thought to predominate in the small patients whereas the thoracic pump is thought to predominate in larger patients. Cardiac Pump- The cardiac pump theory is thought to produce forward flow by direct compression of the ventricles. The direct compression of the ventricles causes increased ventricle to atrial pressure gradient and the competent A-V valves close, and blood is moved out of the ventricles into the aorta- this is artificial ventricular systole. When the ventricle is not compressed the A-V valves open and blood rushes into the ventricles. The cardiac pump is thought to be the primary method of forward flow in patients <15kgs. With the patient in lateral recumbancy perform compressions in patients <15kgs- direct compressions by hand over 5-6 th intercostals space with hand pressure or circumferential palm pressure. Thoracic Pump- The thoracic pump states that forward flow is directly related to changes in intrathoracic pressure from the compressions. As the thoracic cavity is compressed the increased pressure is transmitted differentially to the thick walled arteries vs. the thin walled veins. The thin veins tend to collapse and the thick arteries tend to stay open. The increased thoracic pressure is transmitted to both the intra and extra thoracic arteries but not the veins. Because the veins have valves this prevents backflow of blood. As the compression is released the veins are no longer collapsed- blood rushes into the intrathoracic veins and there is forward flow. In the thoracic pump mechanism the heart acts only as conduit for blood flow and does not serve as a pump at all. The thoracic pump is thought to be more active in patients >15kgs. To perform compressions in dogs >15kgs using the cardiac pump- In lateral recumbancy perform compressions over the widest part of the thorax (NOT over the heart), compress about 30%-50% of the thoracic width, compress with a 1:1 duty cycle (the same amount of time allowed for compression as decompression)- allow the chest to fully recoil and avoid leaning into the compression preventing recoil. Compressions should be administered at a rate of 100-120 compressions per minute in either technique. Closed chest cardiac compressions achieve about 20-30% of normal cardiac output. Uninterrupted chest compressions should continue for 2 minutes after which exchange of rescuers/compressors is recommended to avoid fatigue (One BLS cycle is 2 minutes long). Interposed abdominal counterpressure- thought to increase venous return, and reduce retrograde aortic flow. Complications can include trauma to intraabdominal organs. It is recommended if there are enough rescuers. Open Chest Compressions- Open chest compressions have been shown to increase the cardiac output and forward flow over closed chest compressions especially with concurrent aortic cross clamping. It is indicated if there is no response to closed chest compressions, if there is pericardial 2012 DoveLewis Annual Conference Page 3

effusion or cardiac tamponade, if there is significant flail chest or chest trauma, pleural space disease-pneumo/hemo/hydrothorax, intraoperative arrests where the thorax can be approached through the diaphragm. Open chest compressions should be consider in a setting that has the ability to perform advanced post arrest care and monitoring, and by experienced personnel. Advanced Life Support (ALS)- is defined as the recognition and treatment of arrhythmias including drug therapies, debrillation and fluid therapies Frequency of arresting rhythms in veterinary patients: Pulseless electrical activity (PEA) 23.3% Asystole 22.8% Ventricular Fibrillation 19.8% Sinus Bradycardia 19% This is contrasted with humans in which ventricular fibrillation/pulseless VT accounts for 35-60% of out hospital arrests. Pressor Therapy Epinephrine has historically been the pressor of choice with alpha and beta adrenergic activity. The efficacy is thought to be related to alpha adrenergic vasoconstriction. Beta activity can actually be detrimental contributing to increased myocardial oxygen demand, arrythmogenesis and peripheral vasodilation. Low dose administration (0.01-0.02mg/kg) is recommended after two cycles of BLS (4minutes), high dose administration (0.1-0.2mg/kg) of epi can be attempted if low dose therapy fails. Vasopressin- Has pessor activity at V1 vascular receptors producing a large vasoconstriction and increases aortic pressures and therefore improves cerebral and coronary perfusion pressures. Thought to have activity in acidosis in which catecholamines may be inactive. 0.4-0.8u/kg IV. Use as a substitute or in combinationwith epinephrine. Atropine- Vagolytic- Increased parasympathetic tone or vagal overdrive is thought to play a role in pathology of PEA and asystole, however studies have not shown clear benefit for atropine in these arrest rhythms in people. Because detrimental effect has not been demonstrated atropine at vagolytic doses (0.04mg/kg IV) can be considered in dogs and cats with PEA, high vagal tone and asystle. Electrical Defibrillation indicated for ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT)- Use of biphasic defibrillators is recommended over monophasic defibrillators due to more effective defibrillation at lower energies. Recommended defribrillation energies are- Single monophasic external countershock at 4-6j/kg Single biphasic external countershock at 2-4j/kg Single internal countershock dose is 0.5-1J/kg. Electrical defibrillation should be followed by a cycle of uninterrupted BLS, and then a reassessment of the rhythm. Energy of successive countershock can be increased by 50% if there is not an initial conversion with the first countershock. 2012 DoveLewis Annual Conference Page 4

Lidocaine can incrase the defibrillation threshold (making it harder to defibrillate a patient) and is not recommended for Vfib. But because arrest with VF or VT carries such a poor prognosis lidocaine can be attempted in pulse VT. Magnesum for polymorphic VT (torsade de pointes). Other Therapies NaHCO3- Many Side effects including hypernatremia, hypocalcemia, hyperosmolarity, paradoxic CNS acidosis. Indicated in patients who have arrested with known pre-existing acidosis, in CPCR attempts lasting >10minutes. Calcium Gluconate- Indicated in known hypocalcemic arrests, hyperkalemia, and calcium channel blocker overdose/toxicity. Fluids- Whereas fluids can increase aortic diastolic and mean arterial pressures overzealous fluids usually increase right atrial pressures to a greater extend and thus ultimately decrease coronary perfusion pressures. (Remember that optimizing coronary perfusion pressures is related to improved outcome). Fluids should be administered in known hypovolemia but should otherwise be titrated in other patients. Drug administration during CPR- Central catheter is the best, peripheral forelimb (NOT hindlimb) catheter, intratracheal, IO catheter. When drugs are administered through IT route you should double the dose and administer with 5cc of saline. Drugs administered through peripheral vein should be flushed with 20cc of fluid. Compressions should be continued to try to deliver the drug to the heart. Assessing effectiveness of CPR- EtCO2 >10-15mmHg has been associated with improved survival and increased return of spontaneous circulation in people. Recommended to get EtCO2>15 in dogs, and > 20 in cats. Look at the ECG but also PALPATE for pulses/pulse quality (PEA- can look like any rhythm on the ECG). Post Arrest Care- Up to 68% of patients suffering CPA have been reported to have a rearrest episode. Ventilation/perfusion monitoring, maintaining pressures with vasopressor/inotrope support. Mechanical ventilation may be needed due to increasing PaCO2 and hypoxemia. All organs are target organs for ischemia after an arrest episoderenal function, pulmonary, GUT, brain. Consider mannitol to prevent cerebral edema from ischemia/reperfusion. Control post arrest arrhythmias as they develop. There may a role for mild therapeutic hypothermia for neurologic recovery post CPA. Selected References: Plunkett, SJ; McMichael M. Cardiopulmonary resuscitation in small animal medicine: An update. J Vet Intern Med 2008;22:9-25. Cole SG, Otto CM, Hughes D. Cardiopulmonary cerebral resuscitation in small animalsclinical practice review Part I. J Vet Emer Crit Care 12(4): 2002; pp. 261-267. Cole SG, Otto CM, Hughes D. Cardiopulmonary cerebral resuscitation in small animals-a clinical practice review Part II. J Vet Emer Crit Care 13(1): 2003; pp. 13-23. Haldane S, Marks SL. Cardiopulmonary Cerebral Resuscitation: Techniques. Compendium Oct 2004. p. 780-789. 2012 DoveLewis Annual Conference Page 5

Haldane S, Marks SL. Cardiopulmonary Cerebral Resuscitation: Emergency Drugs and Postresuscitative care. Oct 2004. p. 791-799. Johnson T. Use of Vasopressin in Cardiopulmonary Arrest: Controversy and Promise. Compendium June 2003. p. 448-451. Callaway CW. Chapter 50-Cardiopulmonary Cerebral Resuscitation. In Textbook of Critical Care, Editor Fink: p. 311-324. Kass KH, Haskins SC. Survival following cardiopulmonary resuscitation in dogs and cats. J Vet Emer Crit Care 1992; 2(2): 57-65. Wingfield WE, Van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). J Am Vet Med Assoc 1992; 200(12): 1993-1996. The American heart association website. www.heart.org has links to the new 2010 AHA CPR guidelines or can access through the journal circulation website at http://circ.ahajournals.org/content/122/18_suppl_3.toc For RECOVER initiative guidelines: http://onlinelibrary.wiley.com/doi/10.1111/vec.2012.22.issue-s1/issuetoc http://acvecc-recover.org 2012 DoveLewis Annual Conference Page 6