Update on Small Animal Cardiopulmonary Resuscitation (CPR)- is anything new? DVM, DACVA Objective: Update on the new Small animal guidelines for CPR and a discussion of the 2012 Reassessment Campaign on Veterinary Resuscitation (RECOVER). Cardiopulmonary arrest (CPA) is a dynamic, time-dependent, complex process occurring secondary to failed cardiac contractility, which results in either ventricular asystole, pulseless electrical activity (PEA), pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF). The aims of cardiopulmonary resuscitation (CPR) are to provide maximal blood flow to the heart and brain until restoration of spontaneous circulation. Until recently, veterinary CPR recommendations were largely based on a combination of clinician preference and the ILCOR guidelines. In 2012, the Reassessment Campaign on Veterinary Resuscitation (RECOVER) was designed in order to provide comprehensive CPR guidelines for veterinary medicine. Basic life support (BLS)
In 2010, ILCOR human CPR guidelines changed the order of intervention for all age groups (except newborns) from the classical Airway (A), Breathing (B) and Chest compression (C) - ABC - to Chest compression (C) first, followed by Airway (A) and then Breathing (B) - CAB. This change is in part because securing an airway in humans is fairly challenging and the prolonged intubation time causes a delay in initiation of chest compression, which negatively impacts ROSC. In veterinary medicine however, there is no evidence supporting benefits of CAB resuscitation in comparison to standard ABC resuscitation. When multiple trained rescuers are available, chest compression, securing an airway and ventilation can be initiated almost simultaneously. Chest compression It is essential to provide the highest possible quality chest compression in order to maximize blood flow to the myocardium and brain. CPR guidelines and the 2012 RECOVER veterinary CPR guidelines recommended a compression rate of at least 100 per minute compressing the chest by one-third to one-half of its width to maximize vital organ blood. Myocardial blood flow is determined by the coronary perfusion pressure (C o PP), which is defined as the difference between aortic diastolic and right atrial diastolic pressures. Coronary perfusion pressure can be quantified by the equation: C o PP = DAP - RAP, where DAP is diastolic aortic pressure and RAP is right atrial pressure (diastolic). Institution of effective cardiac compression restores the pressure gradient between the aorta and right atrium, with return of coronary perfusion and a corresponding marked increase in the likelihood of ROSC
If multiple rescuers are present, intermittent abdominal compression (IAC) and chest compression can be performed. IAC has been shown to improve venous return and hemodynamic values in animal CPR models, with little risk to the patient Ventilation During CPR, an open airway should be rapidly established by orotracheal intubation. After the airway is secured, the patient should be ventilated manually with 100% inspired oxygen. No studies have yet evaluated the optimal tidal volume and inspiratory time for dogs and cats during CPR. CPR guidelines currently recommend a ventilation rate of 10 breaths per minute without interruption to chest compression. A full breath should be given in approximately 1 second and with a 10 ml/kg tidal volume. Current guidelines recommend asynchronous ventilation with continuous chest compression. Pharmacological therapy 1. Vasopressors Vasopressors increase systemic vascular resistance, increasing aortic pressure and directing more of the intravascular volume from the peripheral circulation to the central compartment. Chest compression therefore now preferentially perfused the brain and myocardium at the expense of less vital organs. Both epinephrine and vasopressin are a reasonable choice for all types of cardiac arrest. At the correct dosage, epinephrine acts on both alpha (vasoconstrictor) and beta receptors (inotropic and chronotropic) causing increased intracellular calcium and
vascular constriction. An appropriate epinephrine dose regimen is 0.01 mg/kg IV every 3-5 minutes. While a higher dose (0.1 mg/kg) of epinephrine initially increases ROSC, this does not improve hospital discharge rate (survival) and is no longer recommended for CPR. Vasopressin is a non-catecholamine vasopressor that acts on peripheral vessels (V1 receptors), decreasing hyperpolarization and increasing intracellular calcium. In comparison to epinephrine, vasopressin has a longer half life and seems to be a more efficacious vasopressor in a hypoxic, acidotic environment. An appropriate vasopressin dose regimen is 0.8 IU/kg IV every 5 minutes. 2. Anticholinergics The 2010 ILCOR guidelines do not recommend routine use of atropine during CPR. A human CPR study revealed that use of atropine with epinephrine produced a worse outcome than epinephrine alone. In animal CPA after a high vagal tone event (e.g. vomiting, diarrhea), use of atropine is reasonable 3. Buffer therapy The 2010 ILCOR guidelines do not recommend routine use of sodium bicarbonate during CPR. Bicarbonate administration may cause paradoxical cerebral acidosis, hyperosmolarity and decreased catecholamine effectiveness. An appropriate dose of sodium bicarbonate dose is 1-2 meq/kg IV. Bicarbonate use may be considered in prolonged CPA or for CPA due to severe hyperkalemia or severe metabolic acidosis Defibrillation
In the event of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), the recommendation is to start BLS chest compression and then immediately perform electrical conversion (defibrillation). CPR can be frequently interrupted by rhythm check in both the pre-shock and post-shock period; this interruption has a detrimental hemodynamic effect. It is important for the rescuer to understand that BLS compression should resume immediately after shock defibrillation, with no interruption for rhythm check until after a full CPR cycle has been completed. When choosing a defibrillator, preference should be given to biphasic waveform defibrillators. Biphasic defibrillators have been found to be as or more effective than monophasic defibrillators. In comparison to monophasic defibrillators, biphasic defibrillators require less energy for successful defibrillation and produce less tissue trauma and less cardiac damage. Electrical defibrillation should start at 2-5 J/kg with a 50% increase in energy for each subsequent attempt. Post-resuscitation care Hemodynamic optimization To avoid further morbidity, adequate organ perfusion should be established during the post-cardiac arrest phase. Respiratory goals are to maintain a PaO2 of 80-100 mmhg or a saturation of 94-98%. Hyperoxemia (PaO2 >100mmHg) can cause an increase in free radical and neurological injury. It is important to ensure the patient can spontaneous ventilate with a PaCO2 of ~32-43 mmhg. Hypoventilation is common after CPR and long-term positive pressure ventilation
should be available. The major cardiovascular goal is to maintain systolic blood pressure at 100-200 mmhg (mean blood pressure at 80-100 mmhg). Hypotension can be indicative of hypovolemia or decreased vascular resistance. In these cases, use of fluid therapy, inotropes and vasopressors is indicated. Therapeutic hypothermia There is little information about therapeutic hypothermia (TH) for post-cardiac arrest syndrome in veterinary medicine. Advantages of TH include reductions in cerebral oxygen requirement, brain metabolic demand, excitatory neurotransmitters, inflammatory cytokines and free radicals, together with inhibition of neuronal cell apoptosis. Mild hypothermia (97 F) seems to be a safe and logical target. The ideal target temperature and the speed of rewarming the patient have not yet been established in veterinary medicine. Adjunct CPR devices IttP can be manipulated to improve circulation during CPR. Recent advances have been made to maximize decreased IttP during CPR. Examples of these include impedance threshold devices (ITD) and active compression decompression devices (ACD). It is important to remember that use of mechanical CPR devices (i.e. the ITD) has the potential to delay or interrupt CPR for the victim of cardiac arrest. Rescuers should be trained to minimize any interruption to chest compression. In other words, these devices should only be used if they are not a distractor; it is essential
to start immediate chest compression while paying attention to complete and effective chest recoil with adequate ventilation.