CPCR update (Proceedings)

Cardiopulmonary resuscitation (CPR) or cardiopulmonary cerebral resuscitation (CPCR) refers to specific attempts to revive patients who have suffered a cardiac or respiratory arrest, or who otherwise have experienced a severe drop in perfusion pressure (e.g. due to pulseless ventricular tachycardia). The goals of CPCR are to provide continued blood flow and oxygen delivery to the brain and vital organs while attempts are made to restore spontaneous circulation (ie. regain a heart beat). Even in human medicine, success rates for return to spontaneous circulation and hospital discharge following a full cardiac arrest are low, especially if the arrest occurred outside of the hospital setting.  Veterinary medicine has published lower rates of success, but also fewer studies to evaluate CPCR techniques and outcomes.  The development of a plan and a coordinated effort for resuscitation may help to improve outcome results on the veterinary side.  This lecture will address some of the advances in thinking about CPCR that may help to promote better CPCR outcomes. 

A recent study (Hofmeister EH et al. 2009) evaluated 244 episodes of cardiac arrest (161 dogs, 43 cats) at a veterinary teaching hospital.  This study described a successful return of spontaneous circulation in 56 (35%) dogs and 19 (44%) cats.  Despite this modest success, only 9 (6%) dogs and 3 (7%) cats were discharged from the hospital.  The majority of the animals either experienced another cardiac arrest or were euthanized following resuscitation.  In addition to confirming a relatively low rate of discharge from the hospital, this investigation also confirmed prior studies that showed an improved chance of successful resuscitation and discharge if the arrest occurred during anesthesia, as opposed to an arrest that occurred in the ICU or at an out-of-hospital location.

Diagnosis of cardiac arrest is made by observation of a cessation of respiratory activity accompanied by a lack of palpable pulses or auscultable heart beat.  If a cardiac arrest is suspected, the patient should be moved to an area where ECG, blood pressure, intubation devices, and oxygen are available.   Individuals in the immediate area should be alerted, and a division of labor amongst the available helpers should be organized: one person should keep a record; one person may be in charge of drug administration; one in charge of breathing; and one or two people in charge of chest compressions.  The persons performing compressions should switch out regularly (about every 2 minutes) to limit fatigue.

Despite some changes to the recommended algorithm on the human side, the concept of the ABC's (securing an Airway, commencement of Breathing, and then providing Circulation) is still valid in veterinary medicine. Many cardiac arrests in veterinary species are due to respiratory arrest and ensuing hypoxemia and hypercarbia. The first step when trying to revive a patient is to secure a patent airway, usually via endotracheal intubation. A patent airway will bypass any upper airway obstructions that are present, and will allow assisted ventilation if apnea is a contributing cause of the initial arrest. If the cause of arrest is related to pleural space disease (eg. pneumothorax, hydrothorax), a secure airway will not allow adequate ventilation until the pleural space disease is relieved by thoracocentesis or thoracotomy. If there is an upper airway obstruction that cannot be bypassed with an endotracheal tube, the patient will need an emergent tracheostomy to allow intubation and ventilation.  The airway should be secured as soon as possible, so that chest compressions may be commenced.  A slow intubation may compromise overall outcome by delaying the time until compressions can be initiated.

Once a secure airway has been achieved (and verified, either visually, or via observation of chest excursions or end-tidal CO2), the next important aspect of CPR consists of chest compressions. Chest compressions apply outside force to the chest to mimic the pumping function of the heart, and serve to circulate the blood during the period when the heart is stopped. Current guidelines recommend a rate of 120 compressions per minute in humans and small animals. If you are the only person performing CPR, it is more important to continue compressions than to give assisted breaths (ideally, 10-12 breaths are given per minute). Faster, more consistent compressions are more likely to maintain a minimal mean arterial pressure and continued blood flow, as opposed to interrupted compressions, and any interruptions to the compressions (e.g. to verify intubation or to analyze an ECG tracing) should be minimized.  Chest compressions are also necessary to circulate any drugs that have been administered.

What's new in CPCR?

End-tidal CO2 (ETCO2)

ETCO2 is a direct correlate of blood flow through the pulmonary circulation.  In order for CO2 to exchange at the alveoli, blood needs to travel from the tissues to the lungs.  In this context, monitoring of ETCO2 during CPR can provide valuable information about the adequacy of thoracic compressions.  Additionally, when spontaneous circulation resumes, the increased cardiac output will be reflected by an increase in ETCO2.  During CPR, a minimum ETCO2 of 10 – 12 mm Hg is seen with adequate compressions.  Higher ETCO2 during resuscitation, has been associated with a greater chance of the return of spontaneous circulation (Hofmeister EH 2009).  The ETCO2 is also useful for predicting, and hopefully preventing, cardiac arrest; if a precipitous drop in ETCO2 is noted (e.g. in an anesthetized patient), the patient should be examined immediately for a reason to have a decrease in cardiac output, such as surgical hemorrhage.

Vasopressin

The use of pharmacologic agents to augment CPR is a source of controversy and continued research. The main goal of pharmacologic therapy is vasoconstriction, which results in redirection of blood from the periphery to the central compartment.  This shifts flow to the vital organs (heart, brain) and thus supports a return to spontaneous circulation.  Historically, epinephrine has been the first line drug for vasoconstriction; however, epinephrine has both alpha and beta adrenergic effects.  While the alpha agonist effect results in vasoconstriction, the beta effects can result in an increased cardiac workload and higher oxygen demand, which may be detrimental.  Additionally, if an acidosis is present, epinephrine may not have the expected result due to alterations of the target receptors.  

Vasopressin is a drug that causes vasoconstriction via specific V1 receptors in the peripheral vasculature, and has no adrenergic activity, including beta effects.  In addition to the peripheral vasoconstriction, vasopressin seems to result in less constriction of coronary and renal vessels compared to epinephrine.  By maintaining these vessels, vasopressin may help to maintain mycocardial blood flow and coronary perfusion during CPR.  Additionally, vasopressin does not have the arrhythmogenic or chronotropic effects that are associated with epinephrine (primarily due to beta agonism).   While the cardiac workload may be increased somewhat by increased afterload from vasoconstriction, vasopressin does not cause a direct stimulus on the heart to augment myocardial oxygen demand.  There is some evidence to suggest that vasopressin is more effective than epinephrine for cardiopulmonary arrest that initially presents with a cardiac rhythm of asystole (vs. fibrillation), and consequently may be very relevant for use in veterinary patients (few veterinary patients display an initial rhythm of Vfib). For these reasons, vasopressin has become a popular first-line drug during CPCR, given at doses of 0.2 – 0.8 U/kg IV.

Chest Compressions

The latest recommendations from research studies and human medicine emphasize the importance of continuous and rapid chest compressions, initiated as soon as possible after securing an airway (in the case of veterinary species).  The recommended compression rate is 100-120 compressions per minute.  It is also recommended that there be minimal interruptions of the compressions so as not to lose any of the kinetic energy transmitted to the column of stagnant blood.  Compressions should not be stopped for greater than 10 seconds, and at least 2 minutes (and preferably 5 minutes) of continuous compressions should occur between pauses, even to check the ECG rhythm.  The integration of end-tidal CO2 monitoring to resuscitation monitoring will give accurate information about the return of spontaneous circulation that is not subject to interference from motion.   

Impedance threshold device

The airway impedance device or impedance threshold device is a promising new tool which is placed on the end of the endotracheal tube, between the ET tube and the Ambu bag or breathing circuit.  The ITD slows the reexpansion of the lungs during chest compressions, maintaining negative pleural pressure for a longer duration. This negative pressure augments continuous venous flow to the heart before the next compression.  Initial studies in pigs showed that vital organ blood flow (ie. coronary and cerebral perfusion) was significantly higher during CPR performed with the ITD.  Other experimental studies in pigs have shown improved outcome measures as well.  Human studies using the ITD have shown an increased ETCO2, higher coronary perfusion pressure, and higher diastolic blood pressure during CPR.  Other studies have shown that the use of an ITD in out-of-hospital cardiac arrest increases survival to ICU admission, although not necessarily to discharge from the hospital.  

There are few studies of the ITD in small animal patients.  Some studies in dogs with low cardiac output due to anesthesia or hemorrhage have shown that the ITD augments arterial blood pressure, oxygen delivery, and cardiac index, similar to studies in pigs and humans.  The ITD does add resistance to the breathing circuit, and may make it more difficult for smaller patients to breathe spontaneously.

Biphasic defibrillation

Defibrillation is indicated in cases of ventricular fibrillation. An electrical countershock is applied to the heart either across the chest wall. The initial dose is be 3-5 Joules/kg for external, and 0.5-1 J/kg for internal defibrillation. One shock should be delivered, followed by resumption of CPR. If the initial attempts are not successful, CPR should be continued, and defibrillation attempted again after 3-5 minutes, using twice the energy (J/kg) used initially. It is important that the person performing the defibrillation call out “clear” to warn people not to touch the animal or table during defibrillation.

Recently, a new design for defibrillation has been introduced, termed the biphasic defibrillator.  In contrast to the classic monopahsic defibrillator, which sends a shock from one paddle to the other across the thorax, the biphasic defibrillator sends a shock from one paddle to the other, and then another shock back in the opposite direction, effectively applying electricity to the heart twice in a short period of time.  The biphasic defibrillator is advocated because it can achieve similar results (ie. defibrillation) at lower energy levels than the monophasic design.  Although this is true, and the biphasic defibrillator has been used numerous times in small animal patients, the superiority of one waveform over the other has not yet been established, in human or veterinary medicine.

References/Suggested Reading

Cole SG, Otto CM, Hughes D. Cardiopulmonary cerebral resuscitation in small animals- a clinical practice review (part 1 and 2). J Vet Emerg Crit Care 2002; 12(4):261-267 and J Vet Emerg Crit Care 2003; 13(1):13-23.

Hofmeister EH, Brainard BM, Egger CM, Kang S.  Prognostic indicators for dogs and cats with cardiopulmonary arrest treated by cardiopulmonary cerebral resuscitation at a veterinary teaching hospital.  J Am Vet Med Assn. 2009;235(1):50-57.