CPR A Review of Current Practices. The Vet Education Live Web-Seminar (Webinar) Series. Updates in CPR. With Dr Philip Judge

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1 The Vet Education Live Web-Seminar (Webinar) Series 2013 Updates in CPR With Dr Philip Judge BVSc MVS PG Cert Vet Stud MACVSc (Vet. Emergency and Critical Care; Medicine of Dogs) February 20 th 2013 Vet Education is proudly supported by Hill s Pet Nutrition (Australia) and Merial Animal Health 1

2 Special Topic: Updates in Management of Cardiopulmonary Arrest In 2012, the Journal of Veterinary Emergency and Critical Care published a special issue of the journal containing several reviews of the management of patients in cardiopulmonary arrest, based on reviews of scientific literature in humans, laboratory animals and in dogs and cats. The review series culminated in a final article outlining current recommendations for CPR in small animal practice based on documented or suspected improvements in survival rates (1-7). What follows in these notes is a presentation of these recommendations, together with an outline of how your clinic can prepare for cardio-pulmonary arrest, including how to recognize symptoms of impending arrest, and how to monitor the patient following recovery. Causes of Cardiopulmonary Arrest In animals, cardiopulmonary arrest most frequently occurs with diseases of the respiratory system, such as pneumonia, laryngeal paralysis, thoracic effusions, neoplasia, and aspiration pneumonia, as a result of severe multisystem trauma or disease, or in patients with cardiac arrhythmias. In addition, anaesthesia is a particular risk factor for cardio-pulmonary arrest when coupled with any of the predisposing causes listed above. At a cellular and tissue level, predisposing causes of cardiopulmonary arrest may be summarized to include Cellular hypoxia due to tissue injury, poor tissue perfusion, or poor tissue oxygenation Vagal stimulation (incl. during surgery) inducing bradycardia, and hypotension Acid-base and electrolyte abnormalities including disorders such as metabolic acidosis, metabolic alkalosis, hyperkalaemia, hypokalaemia, hypernatraemia and hyponatraemia Anaesthesia anaesthetic drugs are toxicants capable of often-times profound depressions in cardiovascular, respiratory and central nervous system function. If not administered carefully, or when administered to patients with predisposing causes of cardiac arrest, they can produce unpredictable and life-threatening effects. I Have an At Risk Patient What Should I Do? The short answer to this question is to Be Prepared! Being prepared for cardio-pulmonary arrest has several facets, from ensuring that the at risk patient is monitored closely, and receives appropriate therapy for their underlying illness, to ensuring that equipment and staff are prepared to perform effective CPR should the patient arrest. 1. Patient therapy and monitoring it is crucial that critically unwell patients are receiving appropriate therapy for their underlying illness to ensure that tissue cells receive sufficient oxygen for normal function. Monitoring plays a key role in determining the adequacy of therapy. High risk patients should have key parameters monitored on a regular basis, including a. TPR assessments every 30 minutes to 2-4 hrs. It is important to record TPR findings, and to note trends in things such as heart rate, respiratory rate, and mentation and pulse quality. Any abnormal finding should be particularly noted and slated for urgent intervention/action. This particularly applies to any abnormalities of respiratory function, cardiovascular status or mentation, as these three organ systems are crucial for ongoing life. b. Urine output bladder size should be noted, or (preferably), the bladder should be catheterized and urine output measured every 1-2 hrs (depending on the status of the patient). Urine output lower than ml/kg/hr should warrant aggressive diagnostic and therapeutic measures aimed at normalizing urine output 2

3 c. Other monitoring blood pressure, blood testing for coagulation analysis, platelet count, PCV/TP, glucose, blood lactate among others is crucial in addition to clinical observation 2. Equipment for performing CPR it is vitally important that you have all drugs and equipment that may be required to effectively perform CPR readily available and accessible to all members of staff. Many clinics prefer to keep a box or trolley (crash cart) in the treatment area of their hospital, containing all necessary equipment such as ECG monitor, syringes, needles, saline flush, ambu-bags and oxygen source - and drugs to achieve this requirement. Ensure your crash cart or emergency drug kit is regularly serviced and restocked on a daily basis or after each CPR, whichever occurs more frequently 3. Where to perform CPR - Perform CPR in a designated work area you are familiar with depending on your workplace, this will be in the treatment room, theatre, or both. Avoid performing CPR in consultation rooms, wards, or in reception as these locations are typically lacking in equipment that is more readily available in treatment areas or in theatre, such as laryngoscopes, needles, syringes, light sources etc., and the delays in retrieving necessary equipment on a repeated basis can mean the difference between life and death. 1. Training training is essential in order to adequately perform CPR. CPR requires a team approach. In general, a minimum of THREE people trained in resuscitation is required to effectively carry out CPR. Regular training and practice drills involving all staff members should be conducted to ensure an ongoing familiarity with the effective provision of ventilation therapy, chest compressions and appropriate drug therapy. What Are the Warning Signs of Impending Cardiac Arrest? Recognising the warning signs of impending cardiac arrest is crucial (5). Survival rates for CPR can be as low as 3-5% once cardiac arrest has occurred so preventing arrest, by detecting impending arrest, can have a dramatic influence on patient survival. Signs of impending cardiac arrest are generally associated with the respiratory system, cardiovascular system and neurological system, and include Respiration Respiratory rate Decreasing respiratory effort Decreasing tidal volume Changes in respiratory pattern e.g. rapid and shallow to slow and deep; vice versa Pulses and blood pressure Pulse quality variation from regular to irregular pulse amplitude Trend from good pulses to weak pulse quality Hypotension Heart Trend from normal heart rate to bradycardia Trending towards faint heart sounds Anaesthesia Unexplained increases in depth of anaesthesia Mucous membranes Unreliable in assisting detection of impending cardiac arrest Cyanosis is never a good clinical sign and should prompt immediate intervention Note that mucous membrane colour may be normal for several minutes following arrest (!) Level of consciousness Trending toward less arousal Inability to rouse the animal/less responsiveness Pinpoint pupils or dilated, poorly light responsive pupils should cause immediate concern 3

4 What are the Clinical Signs of Cardio-Pulmonary Arrest? Cardiopulmonary arrest symptoms are obvious, and include Inability to rouse the patient Absence of an arterial pulse Apnoea, or the development of an agonal respiratory pattern Dilated pupils Note that dilated, fixed pupils appear 20 seconds, and are maximally dilated within 45 seconds of arrest. This means that patients in cardiac arrest may not always initially show signs of pupillary dilatation NOTE: 1. Loss of pulses occurs with systolic arterial pressure of less than 60mmHg; inability to auscultate the heart occurs when systolic arterial pressure of less than 50 mmhg 2. Pupillary dilation is not a reflection of irreversible neurological damage, and should be used as an indicator of effective therapy, rather than a dictator of when to abandon therapy i.e. do not stop resuscitation just because a patient has dilated pupils - they could recover! 3. CPR should be performed on dead patients if there is any doubt about the duration of arrest. A Crash Cart: This is an image of a crash cart. Note IV fluid bags and oxygen cylinders attached to the cart, along with useful equipment such as scissors, blood pressure cuffs etc., available for immediate access during a resuscitation event. 4

5 Basic Life Support Basic Life Support refers to the first things we do to a patient in cardiac arrest to support airway access, respiratory support and cardiac output, prior to the administration of drugs such as adrenaline etc. Early commencement of basic life support is associated with improved outcome, and is an independent predictor of survival from cardiac arrest (5) Airway Management 1. Extend the head, pull tongue forward, clear pharynx of debris 2. Intubate the patient with an endotracheal tube 3. Suction the airway if necessary 4. If the patient has an oral foreign body, try abdominal and thoracic compressions with the head lowered 5. If laryngeal obstruction prevents intubation, use a tracheal catheter or slash tracheostomy Breathing 1. Evidence suggests that early provision in patients with non-cardiac causes of cardio-pulmonary arrest is beneficial in improving outcomes in CPR (4) 2. Determine breathlessness of the patient over 3-5 seconds 3. After confirmation of the breathlessness of the patient, begin breathing for the patient 4. Ventilation should begin with 2 large breaths, each seconds in duration. If the patient does not begin to breathe within 5-7 seconds, begin ventilating with an ambu-bag and % oxygen at breaths per minute, with a tidal volume of 10 ml/kg, and an inspiratory time of 1-2 seconds (4) Circulation 1. Determine pulselessness of the patient by palpating carotid or femoral pulse; simultaneously auscultate the heart for 5-10 seconds 2. Begin cardiac resuscitation through the provision of cardiac compressions. 3. Some evidence exists in human literature that chest compressions alone may provide sufficient ventilation for the first 4 minutes of resuscitation. Evidence in dogs and cats is unclear on this point, and it is suggested that if chest compressions are applied as the first intervention in basic life support, that endotracheal intubation and ventilation be instituted within the first 4 minutes of resuscitation efforts (4) Cardiac compressions may be provided using external chest compressions or by direct cardiac massage. These cardiac compression techniques will be reviewed below Closed Chest Compressions Closed chest compressions, when performed properly, may achieve cardiac output of between 25-30% of normal cardiac output at best, so adopting the correct technique is critical in achieving the best blood flow and oxygen delivery during CPR (4). During CPR using external chest compression, forward blood flow is initiated usually by one of two mechanisms: The cardiac pump mechanism, and the thoracic pump mechanism Cardiac pump - compression of the chest wall causes compression of the heart chambers and squeezes the ventricles. The cardiac pump is most efficient in small dogs weighing less than 7 kg, and in cats. Narrow chested dogs such as greyhounds may be able to utilize the cardiac pump mechanism. The patient should be in right lateral recumbency, with compression applied directly over the heart, 5

6 with sufficient force to compress the chest to between 30-50% of its resting dimension. The rate of compression should be compressions per minute, with a compression/relaxation ratio of 1:1. Thoracic pump - compression of the chest wall causes increased intra-thoracic pressure, compressing all intra-thoracic structures equally. The result is a forward arterial, and a retrograde venous blood flow. Due to the collapsible nature of thoracic veins, and the venous luminal one-way valves, retrograde blood flow is significantly less than forward flow. The thoracic pump operates to the greatest extent in large dogs. To maximize the thoracic pump mechanism, place the patient in dorsal recumbency, and apply compressions over the distal 1/3 of the sternum, with enough force to compress the thorax 30% of its dimension. Chest compressions should occur at compressions per minute, with a compression/relaxation ratio of 1:1 Ancillary measures for Closed Chest Compressions 1. Ventilate simultaneously with the compressive effort of chest compression - this maximizes intrathoracic pressure and may enhance forward movement of blood. This is known as synchronous high airway pressure ventilation. If a single person is providing CPR, a chest compression-to-ventilation ratio of 30:2 is currently recommended (30 compressions, followed by 2 breaths) (4) 2. Abdominal binding has not been shown to significantly improve forward blood flow from the heart, and is no longer recommended 3. Interposed abdominal counter-pulsation (the abdomen is compressed between chest compressions) may aid in forward blood flow. Animal studies have shown increased coronary blood flow, and carotid blood flow using this treatment (4). If poor pulses are observed with your chosen technique within 2 minutes of initiating CPCR, the procedure should be changed or open chest CPCR initiated Open Chest Direct Cardiac Compression As mentioned above, closed chest cardiac compression achieves only 25-30% of the normal cardiac output flow at best, which is considered less than the minimum flow needed to maintain cerebral metabolism. This is one of the principle reasons attributes to low survival rates, and poor neurological recovery in CPR. Open chest cardiac massage can achieve normal or supra-normal cerebral blood flows, and should be considered in many resuscitation procedures (6). Indications for Open Chest CPCR Intra-operative cardio-pulmonary arrest Hypothermic cardio-pulmonary arrest Inability to generate high intra-thoracic pressures Pneumothorax Diaphragmatic hernia Flail chest Severe patient obesity Pericardial effusion Patients weighing over 20kg Arrest secondary to severe hypotension Multiple trauma Exsanguination Ineffective closed chest compression for greater than 10 minutes 6

7 Open Chest Direct Cardiac Compression: The Technique The technique of achieving open chest cardiac compression is easily learned, and can be completed within 30 seconds of the first incision 1. Have the patient in RIGHT LATERAL RECUMBENCY 2. Make a skin incision with scalpel blade over intercostal space 5-6; curved Mayo scissors are used to incise the intercostal muscles. Beware the intercostal vessels that lie on the cranial and caudal edges of the ribs 3. Weitlaner retractors may be placed to assist rib retraction and enhance visualization of the heart 4. Visualise the heart within the pericardium and provide 5-10 cardiac compressions at a rate of per minute. 5. Perform a sub-total pericardectomy to exteriorize the heart. Incise the pericardium at the apex of the heart, and extend the incision dorsally after visualization of the phrenic nerve. Incision of the pericardium and subsequent exteriorization of the heart has been shown to increase the effectiveness of internal cardiac massage Direct cardiac massage - do not twist the heart; avoid traumatizing or puncturing the heart with fingertips. USE ONLY THE FLAT PALMAR SURFACES OF THE FINGERS. Compress the heart as soon as the ventricle fills. If the target rate of /min cannot be achieved due to slow ventricular filling, slow the rate until venous return is improved through administration of intravenous LRS at 90ml/kg/hr, or hydroxyethyl starch at 5ml/kg administered over 5 minutes, and/or adrenaline/epinephrine administration. Aortic cross-clamping The aorta may be cross-clamped at the descending aorta just caudal to the base of the heart if desired to encourage cranial blood flow and resultant cerebral perfusion. Methods of cross clamping the aorta include using atraumatic clamps, soft 3-5 Fr nasogastric tube, or Penrose drain material tourniquet. This technique increases cranial blood flow. 7

8 Advanced Life Support In order to re-start spontaneous circulation, and to stabilize the cardiopulmonary system and normalize tissue oxygen delivery following basic life support, the techniques of Advanced Life Support are employed. These techniques include the administration of drugs, ECG diagnostics, and defibrillation. Drug Administration Routes of administration Central venous line (jugular catheter) is the route of first choice. However, jugular catheters are seldom in place in cardio-pulmonary arrest patients Tracheal administration drug administration via an endotracheal tube may be considered if intravenous access is not available, and has been shown to be reasonably effective in delivering medications adrenaline, atropine and vasopressin to patients receiving CPR. Importantly, the drug must be given into the carina of the trachea usually delivered via a long urinary catheter. In addition, the dose of adrenaline should be multiplied 10x and diluted 1:1 with sterile water (or 0.9% NaCl) in order to achieve therapeutic serum levels. Follow administration, 3-4 deep positive pressure ventilations should be applied to the patient to assist dissemination of the medication throughout the lung fields. Intra-tracheal administration is contraindicated in patients with pulmonary oedema, and pulmonary disease, and is less effective in patients with intra-thoracic disease or having open chest CPR. NEVER administer bicarbonate via intra-tracheal route, as it destroys alveolar surfactant, reducing lung compliance, and the effectiveness of positive pressure ventilation. Peripheral vein - forelimb only; current research shows that peripheral venous administration is not significantly worse than intra-tracheal administration. Following administration of drugs, the patient should receive an intravenous bolus of 5-10 ml 0.9% sodium chloride to aid in promoting venous transport of the drug to the heart Intraosseous administration of drugs is indicated where venous access is difficult, and in small patients. Drugs are rapidly distributed throughout the vascular system. More effective than peripheral veins or intra-tracheal route Intra-cardiac route is to be avoided as injection into the myocardium can result in refractory ventricular fibrillation Fluid Therapy The rapid infusion of crystalloids, colloids, or blood is indicated if the arrest is due to severe volume depletion. DO NOT USE GLUCOSE CONTAINING FLUIDS. Fluid administration to maintain intravenous lines open is all that is suggested if the patient does not demonstrate volume depletion (3) 8

9 Drug Administration for Patients with Cardio-Pulmonary Arrest Drug types and doses recommended for administration in the advanced life support phase of CPR as a result of the recent RECOVER initiative are as follows Adrenaline 1: DOSE = 0.1 ml/10kg IV q 3-4 minutes, then 1 ml/10kg q 3-4 minutes Indications asystole, severe bradycardia Alternate with vasopressin Contraindicated in tachycardias Vasopressin (DDAVP) - DOSE = 0.3 micrograms/kg (1 ml/25kg) IV q 4 minutes Indications - maintenance of cerebral and coronary blood flow during CPCR Alternate with adrenaline May be superior to adrenaline in hypovolaemia Atropine injection - DOSE = 0.02 mg/kg) 1 ml/30-60kg Repeat in 30 minutes if necessary Indications - sinus bradycardia, ventricular asystole Lignocaine injection 2% - DOSE = 2 mg/kg (1ml/10kg) (cats CAUTION: 0.1 ml/cat) Use in ventricular tachycardia DO NOT USE in ventricular fibrillation Dexamethasone sodium phosphate - DOSE = 2-4 mg/kg IV Use in electromechanical dissociation and idioventricular rhythm Dopamine CRI - DOSE = 5-10 ug/kg/min Indications - sinus bradycardia Sodium Bicarbonate - DOSE = 0.5 meq/kg Indications - Cardiac arrest present for greater than minutes May not provide improvement in survival rates NOT to be given via intra-tracheal route Note: dexamethasone induces release of ATP stores from the mitochondria, despite elevated intracellular calcium, which inhibits this movement. This ATP normalizes cell membrane polarization, and increases camp production. 9

10 Defibrillation In 1899, researchers found that powerful electric shock delivered to the heart in ventricular fibrillation (VF) could convert VF to sinus rhythm. The rationale for this is that a massive electric shock will cause complete depolarization of all individual myocardial fibers. When all cells within a fibrillating heart are depolarized, a condition of electrical homogeneity is established, which is unfavorable to the development of VF. The greater the energy in an electrical shock, the more likely it is to defibrillate a heart. Within animals there is a tremendous variation in the energy required to produce defibrillation, due to variations in intrathoracic impedance. Intra-thoracic impedance (and hence the energy required to defibrillate the heart) are affected by the following Bodyweight Metabolic acidosis Metabolic alkalosis Hypoxia Her- and hypokalemia Hyper- and hypomagnesaemia Digitalis intoxication Antiarrhythmic drugs Acute reperfusion injury Myocardial ischaemia Lignocaine increases the defibrillation threshold by as much as 50%, whereas Aminophylline lowers the defibrillation threshold. The longer an animal has been in ventricular fibrillation, the less successful defibrillation is likely to be. However, all patients stand the best chance of being defibrillated if the energy used for defibrillation is 4-5 Joules/kg (closed chest) Indications for Electrical Defibrillation Ventricular fibrillation - defibrillation precedes basic life support in this instance Rapid ventricular tachycardia that has caused the patient to become pulseless and unresponsive - defibrillation precedes basic life support in this instance Procedure for Electrical Defibrillation It should be noted that only trained personnel that have completed certified training should operate defibrillation equipment, as there is a serious risk of electric shock through improper use. 1. Electrode paddles are coated with gel - particularly around the edges 2. NEVER USE ALCOHOL! 3. Place the paddles on the thoracic wall with enough pressure to compress the thorax - this decreases thoracic impedance. One paddle should be placed at the base of the heart, and the other at the apex. Only 28% of the fibrillating myocardial cells need to be depolarized to cease fibrillation, so absolute positioning is not necessary, especially as the paddle surface is generally as large as the heart. THE PADDLES MUST NOT TOUCH EACH OTHER. 4. Charge the paddles to 4-5 J/kg 5. Ensure no one is in contact with the animal, the table, or is standing on a wet floor in the vicinity 6. The operator inspects the scene, and loudly announces ALL CLEAR, and discharges the defibrillator 7. If the first shock fails to convert the rhythm to a haemodynamically stable one, a second shock of equal energy should be given. If this fails, a third shock with increased voltage should be administered. If no response occurs, causes of increased trans-thoracic impedance such as pneumothorax should be suspected, and investigated. Epinephrine may also be used to lower the defibrillation threshold. 10

11 Electrocardiography Electrocardiograph (ECG) diagnosis of arrhythmias at the time of arrest is essential to ensure correct and rapid drug therapy is instituted Ventricular asystole Complete absence of ECG complexes - the so-called flat line Indicative of cardiac arrest with severe underlying disease, and implies a poor prognosis Treatment Basic Life Support Adrenaline +/- vasopressin Atropine Precordial thump - if nothing else, it makes you feel better! Fig 1: An ECG tracing showing a normal QRS complex, a large T-wave followed by asystole Sinus Bradycardia Slow heart rate - dogs < 60 bpm, cats < 140 bpm Aetiology - hypothermia, anaesthetic drugs, increased vagal nerve tone Treatment Atropine 0.04 mg/kg SLOW IV Dopamine 5-10 ug/kg/min IV Fig 2: An ECG tracing showing profound sinus bradycardia 11

12 Sinus Tachycardia Rapid heart rate - dogs > 160 bpm, cats > 240 bpm Treatment - treat the cause; e.g. pain, hypoxia, hypotension etc. Fig 3: An ECG tracing showing sinus tachycardia. Note the wandering baseline undulations caused by the patient s respiratory efforts Ventricular Tachycardia Develops when one or more ectopic foci in the myocardium depolarize repetitively, producing > 3 ventricular premature depolarization's in a row. The QRS complexes are widened and bizarre, with an increased height/amplitude on the ECG tracing. The T wave is also large, and is usually opposite the QRS depolarization direction on the ECG tracing Aetiology - primary cardiac disease, hypoxia, electrolyte abnormalities, following ischaemic disease (pancreatitis, snake bite, gastric dilatation-volvulus etc) Treatment Lignocaine bolus 1-2 mg/kg IV (dog), followed by constant rate infusion of ug/kg/min Defibrillation as last resort Fig 4: An ECG tracing showing ventricular tachycardia. Note the wide, bizarre QRS complexes typical of ventricular tachycardia. In this tracing, P-waves begin to emerge in the final 3 complexes. A slow ventricular tachycardia is often referred to as an accelerated idioventricular rhythm, and at a rate of beats per minute, may not require antiarrhythmic therapy in order to sustain normal cardiac output. Electrolyte levels, analgesia, acid-base status and hypovolaemia should be corrected in this patient prior to anti-arrhythmic agents 12

13 Electromechanical Dissociation Normal ECG tracing in many cases, but there are no palpable pulses, and no heart sounds. Indicates very low blood pressure, very weak cardiac muscle contractions, or complete dissociation of electric and mechanical activity in the heart Pulseless idioventricular rhythm - is a form of electromechanical dissociation, where ECG tracings indicate the complexes are from ventricular origin. The QRS complexes are wide, the heart rate is slow, and there are no P waves. This arrhythmia is associated with severe metabolic or cardiac disease, and carries a poor prognosis Treatment Adrenaline +/- DDAVP Dexamethasone sodium phosphate Basic life support if accompanied by cardio-pulmonary arrest Fig 5: An ECG tracing of electro-mechanical dissociation. This ECG tracing will not result in palpable pulses or audible heart sounds on thoracic auscultation 13

14 CPR A Review of Current Practices Ventricular Fibrillation Is a disordered electrical activity within the heart muscle, resulting in ineffectual contraction, and cessation of cardiac output. There is a characteristic saw tooth appearance to the fibrillation waves on ECG. Coarse ventricular fibrillation has greater deflections than fine ventricular fibrillation. Treatment Basic life support Adrenaline to convert fine ventricular fibrillation to coarse ventricular fibrillation Defibrillation counter-shock ASAP at 5-6 Joules/kg Fine and course ventricular fibrillation 14

15 CPR A Review of Current Practices Post-Resuscitation Management (3) Maintain normal blood pressure, heart rate, and cardiac rhythm with fluid therapy, positive inotropes, and appropriate antiarrhythmic therapy Provide oxygen supplementation via nasal oxygen catheter Provide ventilatory assistance as indicated. It is preferable to monitor end-tidal carbon dioxide concentrations, and to provide intermittent positive pressure ventilation if the ET carbon dioxide concentration rises above 45 mm Hg Turn patient every 2 hours Elevate head 30 deg above the horizontal plane Control seizures with diazepam as required Maintain normal to slightly low body temperature Monitor hydration status and electrolyte levels If the patient deteriorates neurologically, or show signs of cerebral oedema, manage with fluid therapy, mannitol etc. as indicated Insert urinary catheter and monitor urine output - aim for 2-4 ml/kg/hr NB - seizures post resuscitation are not uncommon. Status epilepticus is a poor prognostic sign; small focal seizures do not correlate with a poor prognosis. References 1. Boller M, Fletcher DJ. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 1: Evidence analysis and consensus process: collaborative path toward small animal CPR guidelines. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S4-S Brainard BM, Boller M, Fletcher DJ. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 5: Monitoring. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S65-S Fletcher DJ, Boller M, Brainard BM, Haskins SC, Hopper K, McMichael MA, et al. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 7: Clinical guidelines. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S102-S Hopper K, Epstein SE, Fletcher DJ, Boller M. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 3: Basic life support. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S26-S McMichael M, Herring J, Fletcher DJ, Boller M. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 2: Preparedness and prevention. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S13-S Rozanski EA, Rush JE, Buckley GJ, Fletcher DJ, Boller M. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 4: Advanced life support. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S44-S Smarick SD, Haskins SC, Boller M, Fletcher DJ. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 6: Post-cardiac arrest care. Journal of Veterinary Emergency and Critical Care. 2012;22(s1):S85-S