CPCR update: it may take your breath away (Proceedings)
The first published article on cardiopulmonary cerebral resuscitation (CPCR) was published over 50 years ago, entitled "Closed-Chest Cardiac Massage" and was published in the Journal of the American Medical Association (Kouwenhoven, 1960). Despite this long history, even today CPCR is unsuccessful in the vast majority of attempts. While patient selection undoubtedly plays a significant role in determining outcome of CPCR, such that efforts are more successful when promptly applied to patients with electrical instability, but exceedingly ineffective when used in chronically debilitated patients and those suffering arrest as part of an advanced illness, recent reports have emphasized the limitations in the quality of CPCR. It is with this impetus that there has been a renewed interest in how we perform CPCR that has brought about some important recommended changes in CPCR procedure guidelines. Initial guideline changes were presented in 2005, but have just recently been fine-tuned in December of 2010. Some additional recent advances have also been placed on how to monitor CPCR efforts, which may help to stimulate real-time modifications in CPCR efforts, and possibly improve survival.
Basic & advanced life support
The ABCs (airway, breathing and circulation) of basic life support include achieving a patent airway, delivering periodic, manual lung inflations and promoting circulation with chest compressions. In veterinary patients, tracheal intubation (which is considered a component of advanced life support) is the predominant method of maintaining a patent airway for in-hospital patients. The endotracheal tube is typically attached to a self-inflating bag (or AMBU bag - Airway, Mask and Breathing Unit) to provide manual respirations. If available, it is encouraged to provide continuous oxygen flow into the AMBU bag, and therefore the patient, with each breath. It has recently been discovered that there is a significant tendency to over-ventilate cardiopulmonary arrest (CPA) patients. It is not uncommon for trained health care workers to be observed ventilating CPA patients at 20-30 breaths/min (bpm), despite the current recommendations of 8-10 bpm. These manually delivered respirations, unlike spontaneous breathing, inflate the lungs by providing positive intrathoracic pressure. This increase in intrathoracic pressure deleteriously impedes venous return to the thorax, thus decreasing ventricular filling. Inadequate ventricular filling limits the ability of chest compressions to provide sufficient cardiac output in this no or low-flow state. High intrathoracic pressures can also reduce coronary perfusion pressure (see below). It is not only elevated respiratory rates, but also increased tidal volumes that may be deleterious. Current tidal volume advised during CPCR is 6-7 ml/kg, which is typically of sufficient volume to elicit a visible rise and fall of the thoracic wall with each breath. It is important to know that pediatric AMBU bags and adult AMBU bags have tidal volumes of 450-500 mls and 1100-1600 mls, respectively. Patients with agonal respirations have been shown to be associated with improved survival. This improved survival is presumably due to the negative intrathoracic pressure generated with each breath, aiding preload. These respirations should be included in the respiratory count per minute. The recommendations of manually delivered breaths/min and tidal volumes may need to be increased in patients who experience CPA because of a respiratory cause.Chest compressions are essential in CPCR. Chest compressions are performed with the intent to restore cardiac output and thus maintain organ perfusion. A primary focus is to maintain perfusion to the target organs – the myocardium via coronary arteries and the brain via cerebral arteries. It is known that coronary perfusion pressure (CPP), which is the difference between aortic pressure in diastole and right atrial pressure, is a prime determinant of whether a patient develops a return of spontaneous circulation (ROSC). There are currently two different, commonly used methods of performing chest compressions in veterinary patients, direct cardiac compression (cardiac pump) and indirect thoracic compression (thoracic pump). The cardiac pump, generally recommended in patients weighing less than 15 kg, provides antegrade flow via direct compression of the heart chambers with the heart valves helping to prevent retrograde flow. In patients weighing more than 15 kg, the thoracic pump is recommended. In contrast to the cardiac pump, the thoracic pump provides antegrade flow by globally increasing intrathoracic pressure and secondary compression of the great vessels. The heart acts as a passive conduit for the blood to flow through it.
The rate of chest compressions should be 100-120 bpm, forceful enough to displace the thoracic diameter about 20-30%, with compression:decompression ratio of 1:1, that is equal time for each phase. It is vitally important for the decompression phase to be complete, thus allowing maximal ventricular filling prior to the next compression. Incomplete thoracic recoil occurs most commonly when rescuers fatigue and begin to lean on the patient. Chest compressions should be provided continuously, as experimental data suggests that as little as 10 s of interruption to chest compressions compromises patient outcomes. Recent studies have shown that it is common for complimentary maneuvers to disrupt chest compressions for as much as 27-54% of the CPCR period. These maneuvers may include attaching monitors, endotracheal intubation, defibrillation, rhythm evaluation, establishing vascular access, medication administration (if endotracheal) and ventilations in out-of-hospital resuscitation attempts. It should be emphasized therefore, that these maneuvers be performed in a rapid, efficient manner to minimize interruptions in chest compression. For this same reason, it should be no longer recommended to stop chest compressions to deliver manual respirations.
In an attempt to enhance the therapeutic benefits of chest compressions, the concept of active compression decompression (ACD) CPCR has been developed. This concept was inspired by a patient who was successfully resuscitated with the use of a household plunger (Lurie, 1990). Active compression decompression is performed with a device that includes a suction cup, effectively transforming the chest into an active bellows, where compressions force blood out of the thorax and decompression or recoil draws blood back into the thorax. Active compression decompression augments the naturally occurring, negative, intrathoracic pressure by physically expanding the chest wall and returning it to its resting position. Several factors can contribute to a decrease in the inherent thoracic wall recoil. These include age, rib fractures, barrel-shaped thorax, pectus excavatum and an incomplete release of pressure by the rescuer. Further contributing to loss of the potential hemodynamic benefit of this negative intrathoracic pressure (vacuum) is lost by the rapid equilibrium of airway pressure with atmospheric pressures, by the influx of respiratory gas. In an attempt to prevent this rapid equilibration in airway pressure, and therefore rapid resolution of the intrathoracic vacuum, the inspiratory impedance threshold device (ITD) was developed. The ITD has pressure-sensitive valves that selectively impede an influx of inspiratory gas during thoracic wall decompression, thereby augmenting the amplitude and duration of the vacuum within the thorax. This heightened and sustained intrathoracic vacuum, draws more venous blood into the heart, improving preload and therefore stroke volume. It has been documented that each positive-pressure ventilation will obliterate the negative intrathoracic pressure that has been produced by the ITD, therefore requiring regeneration post-manual respiration. Thus, the lower the manual respiratory rate, the greater blood flows back to the heart. An added benefit is the LED signal that displays when to breath. The Food and Drug Administration has approved the ITD as a circulatory enhancer device, while the ACD CPCR device has yet to be approved. The ITD can be used with any method of CPCR that involves external chest compressions.