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.

Although there have been no prospective studies that clarify the role that open-chest cardiac compressions play in CPCR, in addition to being utilized as a salvage procedure if external cardiac compressions fail, other indications include pericardial disease (pericardial effusion, peritoneopericardial diaphragmatic hernia), presence of rib fractures and pleural space disease (pleural effusion, diaphragmatic hernia, etc). Additional measures, such as hemorrhage control (if previous trauma or hemothorax) and descending aortic cross-clamping (to promote "forward flow" to the brain and heart) may prove beneficial on a case-by-case basis. The decision ultimately lies in the clinician's hands as to when the increased morbidity associated with this procedure makes it justified to pursue. Direct cardiac massage is obviously recommended when CPA occurs during a laparotomy or concurrent thoracotomy.

Defibrillation remains the treatment of choice for ventricular tachycardia and ventricular fibrillation. The effective strength (measured in joules) of electric shocks depends on the waveform delivered. Newer, biphasic defibrillators, are effective at lower joules (lower energy) than older, monophasic defibrillators. This lower energy may limit injury to myocytes that is inherent to the electrical current being delivered during defibrillation. The traditional practice of administering up to three successive (stacked) shocks has fallen out of favor. Major shortcomings of this strategy are the interruption of chest compressions (studies reveal up to 37 second delay to administer 3 shocks), during which there is a detrimental decline in coronary perfusion, as well as an exacerbation of myocardial injury. Because of the necessity to temporarily interrupt CPCR, a single-shock protocol is now preferred. The single shock strategy places an emphasis on minimizing the preshock pause (interval between stopping chest compressions and delivering a shock), the application of a single defibrillation, followed immediately by about two minutes of quality chest compressions before subsequent shocks are delivered.

While establishing IV access is important during CPCR for the administration of medications, it should not occur at the expense of performing chest compressions. Therefore, peripheral venous access may be preferred over central venous access, because the latter commonly requires disruption in CPCR efforts. It is important to follow the administration of IV medications through a peripheral line with sufficient crystalloids to centralize the medications (hence a forelimb may therefore be preferred to a hindlimb). If IV access is not available, then intraosseous administration is the next alternative, with the endotracheal route being the last alternative. The latter route of administration has the most erratic absorption. Medications that can be given via the ET route, include the NAVEL drugs; naloxone, atropine, vasopressin, epinephrine, and lidocaine. Endotracheal administration is best absorbed if deposited at the level of the lower airways, warranting dosage increases that are 2-2.5 times that administered IV with some studies suggesting the required dose of epinephrine given ET to be 3 to 10 times higher than the equipotent IV dose. The administered ET medications should be given with up to 10 mls of sterile water and flushed with several brisk ventilations. Sterile water has been shown to be superior to sterile saline in some studies. Intracardiac administration of medications is no longer recommended.

Despite the universal use of vasopressor therapy (epinephrine and vasopressin), and persistent practice of administering other classes of medications (anti-cholinergics [atropine], anti-arrhythmics [lidocaine, etc.], calcium supplements [calcium gluconate], buffers [sodium bicarbonate], etc.) during CPA, there is little to no evidence that these medications improve survival in the general CPA population. Administration of vasopressor medications is still advised in select CPA patients, with the intent to promote systemic vasoconstriction, redirecting blood flow to the coronary and cerebral circulation. Current recommendations are to administer low-dose epinephrine first, followed by either a second dose of epinephrine or vasopressin. Other medications may provide benefit in special circumstances. Atropine is no longer advised for routine use, but remains the first line drug for acute, symptomatic bradycardias. Calcium gluconate may be beneficial in patients who experiencing hyperkalemia or hypermagnesemia, or are receiving calcium channel blockers. Sodium bicarbonate may be advised in patients experiencing CPA due to hyperkalemia, cyclic anti-depressant overdose, or have a severe metabolic acidosis.

Although the rapid administration of large volumes of IV crystalloids may be traditional for CPA patients, this practice may have a deleterious impact. Volume expansion with IV fluids causes an increase in right atrial pressures, with little impact on aortic pressures, therefore possibly compromising CPP. In general, IV fluid loading should be limited to patients that present with volume depletion. If a crystalloid is to be administered, unless there is documented hypoglycemia, the crystalloid should be a non-dextrose containing fluid. The latter recommendation stems from the knowledge that non-survivors of CPA have a higher incidence of hyperglycemia.

Monitoring

There are a number of approaches used to gauge the quality of CPCR being provided. A few, simple, real-time monitoring techniques include observation of procedures – such as rate, depth and positioning of compressions; rate and depth of ventilation; endotracheal intubation, etc. – detection of pulses, blood gas interpretation, electrocardiographic (ECG) monitoring (rhythm and morphology), and end-tidal CO2 (ETCO2).

Although arterial pulse and pressure evaluation are simple procedures, they are not reliable markers of blood flow during CPCR due to the presence of retrograde pressure through the venous system being incorrectly interpreted as arterial pulsations. The use of a Doppler crystal on the cornea, in an attempt to detect retinal pulses, is fraught with the same inadequacies as manual palpations. Patient movements may also cause "false positive" pulse detections secondary to movement artifact with either technique.

Blood-gas measurements of PCO2 may give some guidance of ventilation during cardiac arrest, but there is often a respiratory alkalosis on the arterial side (due to limited pulmonary blood flow and delivery of CO2), and a respiratory acidosis on the venous side. The other concern with this monitoring tool is that the information obtained is only intermittent and not a continuous monitoring tool.

ECG monitoring is essential for interpreting the electrical activity of the heart. Interpretation of the ECG requires temporary disruption in chest compressions and therefore has an adverse influence on ROSC. Therefore, it is recommended that other means of monitoring for forward blood flow be utilized.

End-tidal CO2 provides a measurement of pulmonary blood flow, and therefore has emerged as a very good measure for quantifying the "cardiac output" produced by chest compression. We know that end-tidal CO2 levels fall immediately at the onset of cardiac arrest, while they also increase with the initiation of chest compressions, providing a linear correlation with cardiac index (when alveolar ventilation is stable), predict successful resuscitation (when able to maintain a level exceeding 25% of baseline) and allow detection of ROSC when a sudden increase in the ETCO2 level occurred (Gudipati, 1998). As a surrogate for cardiac output, it not only helps detect quality of compressions, but also helps detect operator fatigue, which may occur within 1-2 minutes after a rescuer starts chest compressions. This necessitates frequent circulation of team members to help minimize ineffective precordial compressions. Implementation of ETCO2 as a monitoring device also allows for rapid detection of ROSC, without disrupting compressions to evaluate ECG tracings or palpate for a potentially pulsatile rhythm. In fact, the 2005 American Heart Association guidelines state that "although ETCO2 serves as an indicator of cardiac output produced by chest compressions, and may indicate ROSC, there is little other technology available to provide real-time feedback on the effectively of CPR". Human studies have confirmed the prognostic value of ETCO2, while the first sign of ROSC was a rise in end-tidal CO2.

Therapeutic hypothermia

Early studies are suggestive that induced hypothermia (in an attempt to limit oxygen requirements of metabolic tissues) may help minimize the severe neurologic impairment that occurs with cerebral ischemia secondary to cardiac arrest. Hypothermia commonly occurs passively during CPCR, but may be actively promoted by the administration of cold crystalloid fluids. Although definitive recommendations for induced hypothermia cannot be made at this time, what is clear from this data is that aggressive rewarming and hyperthermia should be avoided.

References

ECC Committee, Subcommittee and Task Force of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S640-S946. OR http://circ.ahajournals.org/content/vol122/18_suppl_3/.

Cabrini L, Beccaria P, Landoni G, et al. Impact of impedance threshold devices on cardiopulmonary resuscitation: A systemic review and meta-analysis of randomized controlled studies. Crit Care Med 2008;36:1625.

Gudipati CV, Weil MH, Bisera J, et al. Expired carbon dioxide and pH gradients during cardiac arrest. Circulation 1986;74:1071-1074.

Kouwenhoven WB, Ing Jude JR, Knickerbocker GG. Closed chest cardiac massage. JAMA 1960;173:1064-1067.

Lurie KG, Lindo C, Chin J. CPR: the P stands for plumber's help. JAMA 1990;263:1661.

Plunkett SJ, McMichael M. Cardiopulmonary resuscitation in small animal medicine: An update. J Vet Intern Med 2008;22:9-25.