“Medic 452, EMS 48, Engine 57, Respond Code 3 to a subject down in front of the arcade. 200 Meadowlark Shopping Center, 124th at 82nd Avenue.”
On arrival, the two ambulance paramedics and EMS chief find a 54-year-old male unconscious and unresponsive. The patient is laying supine on the sidewalk, with bystander CPR in progress. Witnesses report the man collapsed suddenly to the ground, and was determined apneic and pulseless by a bystander.
Compressions-only CPR was initiated immediately. Witnesses further report that compressions have continued, uninterrupted, since determination of cardiac arrest three minutes prior.
As the bystander continues to provide compressions, one paramedic assembles a bag-valve mask (BVM) while the other begins to cut away the patient’s clothing. The EMS chief powers up the monitor/defibrillator. By the time the chief places defibrillation pads on the patient’s chest, one of the two first-in paramedics has taken over the resuscitation effort from the bystander and is continuing to provide uninterrupted compressions. The engine has now arrived on scene with three BLS personnel, and its crew is directed to move into position at the patient’s airway.
One of the EMTs positions himself at the crown of the patient’s head, opens the airway and maintains an effective mask seal with a two-handed technique. The other EMT delivers a brief ventilation equal to approximately 300 cc total ventilatory volume, supplemented with 100% oxygen, on the upstroke of every 10th compression. Crew members rotate frequently to avoid rescuer fatigue while compressions continue, uninterrupted, as they have from the moment of collapse.
The ECG shows the patient to be in coarse v fib. Just over four minutes post-arrest, the patient is defibrillated at 200 J, and compressions are resumed immediately. A single, low-volume ventilation continues to be provided on the upstroke of every 10th compression. One minute later, the patient’s end-tidal carbon dioxide (EtCO2) is noted to be 40 mmHg and blood oxygen saturation (SpO2) is at 74%. These values continue to increase over the next minute. Two minutes post-defibrillation, the ECG shows a narrow complex bradycardia. Peripheral pulses are present at a rate of 50, weak and regular, and spontaneous respirations are at a rate of 12 and regular, with adequate tidal volume are also noted.
The patient is transported to a regional cardiac center, where he’s evaluated and admitted for observation. Three days later, he’s discharged from the hospital without functional impairment.
“Cardiopulmonary resuscitation”—the name itself leaves no doubt as to the importance of both the heart and the lungs in achieving our ultimate goal of delivering oxygen to tissues. Nevertheless, the recalibration of resuscitation priorities in the last several years—with an emphasis on optimizing coronary and cerebral perfusion as the single most critical component—has led to some confusion, skepticism and outright controversy. In this article, we hope to shed some light on the physiology of resuscitation and how not only a new appreciation of the importance of CPR itself, but also how the application of newer techniques, such as hands-only CPR and upstroke ventilation, might play a role in achieving better patient outcomes.
The 2005 American Heart Association/International Liaison Committee on Resuscitation guidelines represented a renaissance in emergency care, with a return to CPR as the foundation of successful resuscitation from cardiopulmonary arrest. This back-to-basics approach represented a recognition of the importance of high-quality CPR in restoring circulation for non-shockable rhythms and preparing the fibrillating heart for successful countershock. In addition, the need to emphasize high-quality CPR also reflected the increasing realization that current performance was suboptimal and that, perhaps, the focus on advanced airway and vascular access and delivery of medications was distracting rescuers from basic life support techniques.
So what’s the problem, and why the controversy? First, we must understand the physiology of CPR and the interaction between compressions and ventilations. With spontaneous ventilation, negative pressure is generated by chest cavity expansion, which pulls in not only air through the nose and mouth but also blood from the rest of the body, enhancing venous return and cardiac output. During the performance of CPR, however, the delivery of a breath occurs via positive-pressure ventilation, which increases pressure in the thorax and actually inhibits venous return and cardiac output. This pressure can be extreme with excessively fast ventilation rates, which are unfortunately common during resuscitation. In addition, the interruption in compressions that’s recommended with an unprotected airway results in an immediate drop in cardiac output and mean arterial pressure. The 2005 guidelines addressed these issues by changing the recommended ratio of compressions to ventilations to 30:2, which minimized interruptions and decreased ventilation rates. However, even with “perfect” CPR (e.g., 100 compressions per minute, with a five-second pause in compressions to deliver two breaths, and a five-second pause every two minutes for rhythm analysis), the compression fraction—the percentage of time during arrest that compressions are being performed—can only be about 70%.
It’s notable that the adoption of the 2005 guidelines didn’t result in dramatic, across-the-board improvements in survival as anticipated. However, several notable exceptions emerged in both the out-of-hospital and inpatient environments. In each case, these success stories involve an even greater emphasis on perfusion (i.e., compressions) over oxygenation/ventilation. This in turn has yielded a significant increase in patients not only surviving cardiac arrest, but in leaving the hospital neurologically intact.1,6
Perhaps the most visible example of this focus on compressions over ventilations has occurred in the Arizona out-of-hospital environment. More than a decade ago—and well before the 2005 guidelines were published—the Arizona State EMS Authority implemented a program in which compression-only CPR was performed upon arrival of EMS personnel and for the first three cycles of compressions/rhythm analysis/defibrillation. As a result of this dramatic change in CPR performance, survival from out-of-hospital cardiac arrest rose dramatically throughout Arizona, particularly among patients with v fib. As Arizona State EMS Medical Director Bentley Bobrow stated in a 2008 study of ventilation rate and duration:
“The physiological penalty of assisted ventilation, with its frequently incorrect rate and duration, is a persistently positive intrathoracic pressure throughout the decompression phase of CPR. This decreases cardiac preload, cardiac output, and hinders right ventricular function.”4
Although the results in Arizona were compelling, they begged the question as to whether ventilations during CPR were always counterproductive or if they should be used only for patients in whom a lack of oxygen might be part of the etiology of the arrest in the first place, or could help restore spontaneous perfusion.
For this we must look to the published literature. Beginning in the 1990s, research efforts suggested ventilation during resuscitation was perhaps not as important as previously assumed.2,3 Some authors even concluded that ventilations—particularly when excessive—might even be harmful.4,7 Rat models of arrest documented no significant survival differences between animals receiving and not receiving mechanical ventilation during cardiac arrest, despite a measurable increase in arterial pO2 and decrease in pCO2 among ventilated animals.2 Similar results were observed in porcine models of cardiac arrest, with no difference in 24-hour survival.3,9,10 One study even documented that arterial oxygen content remained essentially unchanged for up to five minutes following cardiac arrest, challenging the need for any ventilations during the initial stages of resuscitation.8 Other investigators suggested the presence of gasping respirations during cardiac arrest are sufficient to maintain arterial pCO2 and pO2 values, obviating the need for supplemental ventilation.5
Does this put the issue to rest? It’s important to realize that the vast majority of animal models use the induction of v fib to produce a state of arrest. In this situation, it’s likely that adequate oxygen stores are present at the time of arrest to adequately supply vital tissues, as long as adequate perfusion is maintained.
But what about patients who are hypoxic during the resuscitation—particularly those in whom asphyxia might be the actual cause of arrest? The Arizona experience doesn’t help much here, as patients with non-shockable rhythms did extremely poorly before and after their transition to compression-only CPR. In addition, patients with obvious asphyxiation, such as hanging or drowning victims, were excluded from the compression-only protocols.
To help answer the question about a role for intra-arrest ventilations for certain patients, we can turn to the inpatient environment, where many patients suffer arrest due to hypoxia. At the University of California at San Diego, we developed the Advanced Resuscitation Training (ART) program in 2007. The ART program gave us the flexibility to modify resuscitation protocols based on our patient population, performance improvement data and the technology available to our providers.
As part of the initial implementation of the ART program, we decided to teach continuous chest compressions but—knowing asphyxia was a common cause of our arrests—with a ventilation administered every 10th compression. The ventilation was timed with the upstroke of the preceding compression, which leaves only about 3/10 of a second in which to deliver a breath.
To determine whether this was scientifically and clinically feasible, we first evaluated the original evidence suggesting a full second was required for each ventilation, particularly with an unprotected airway.
These studies were performed using a cadaver model and documented that a ventilation delivered too quickly resulted in airway pressures that exceeded esophageal sphincter ability to prevent gastric insufflation. Of note, however, was the fact that no compressions were being performed.
We hypothesized chest recoil would actually favor pulmonary inflation and allow adequate tidal volumes to be performed. We then studied this possibility in the San Diego out-of-hospital environment by using capnography to estimate tidal volumes before and after intubation during performance of CPR.
Using various mathematical models of ventilation, we demonstrated that tidal volumes were actually quite similar with BVM ventilation and via an endotracheal tube. In addition, aspiration events due to regurgitation of stomach contents—one of the feared complications of gastric insufflation—weren’t reported following implementation of this protocol.
We estimated tidal volumes were approximately 300 cc, which may be sufficient to provide oxygenation without leading to excessively high intrathoracic pressures as might be observed with 800 cc tidal volumes.
Ultimately, however, the best clinical evidence came from our hospital outcomes, which improved dramatically following ART program implementation. Overall survival increased 2–3 times across all arrest victims. However, among patients with a documented asphyxial arrest—who we speculated would be the most vulnerable to inadequate tidal volumes during CPR—we observed a quadrupling of survival-to-hospital discharge rates following application of our upstroke ventilation protocol.
In addition, we haven’t observed a rebound hypercapnia with EtCO2 monitoring following return of spontaneous circulation (ROSC). Similar success has been observed in Ventura County (Calif,) EMS, where early data following implementation of the ART program has produced some of the best survival rates for out-of-hospital cardiopulmonary arrest ever reported.
Together, these pieces of evidence suggest that it’s possible to provide adequate oxygenation and ventilation to patients in whom the need for oxygenation during arrest resuscitation is suspected.
So where does that leave us? It’s difficult to separate the independent effects of upstroke ventilation as part of the ART program, which involved multiple protocol changes and modifications to training and equipment all at once. Even in Arizona, compression-only CPR was part of a bundle of care changes designed to enhance perfusion above everything else.
Clearly, more research is required to explore questions such as:
1. Are continuous compressions—with or without ventilations—superior to interrupted compressions during CPR?
2. Which patients benefit from upstroke ventilations during continuous compressions?
3. What’s the optimal ratio of compressions to ventilations?
Until these questions are answered, we believe the existing data supports two important concepts. First, agencies and hospitals that decide to adopt continuous compression protocols are justified in doing so. Second, agencies/hospitals that have concerns about abandoning ventilations altogether may consider teaching upstroke ventilation as an alternative to compression-only approaches. This may be applied to all patients, those with non-shockable rhythms or to suspected asphyxial arrest victims.
An upstroke ventilation protocol can be simplified into several key elements. Upon determination of an arrest state, chest compressions are initiated at a rate of 100/ minute. On the upstroke of every 10th compression, a low-volume ventilation (approximately to approximately 300 cc) is rapidly delivered. This works best with one rescuer holding the mask and another squeezing the bag with two hands. This results in a ventilation rate of 10 breaths per minute. While timing a breath with the upstroke of a compression may seem challenging, the rescuer can actually begin squeezing the bag as the compressor reaches the bottom of a compression and rely on the sudden drop in intrathoracic pressure to iniate each breath. Emphasis on high-quality compressions is critical to ensure appropriate rates and allow full recoil—and maximum negative intra-thoracic pressure during upstroke—to optimize ventilation.
Upstroke ventilation is a promising approach that may allow us to accomplish three important goals simultaneously:
1. Maintain coronary and cerebral perfusion pressures through elimination of regular interruption of chest compressions;
2. Minimize increases in intrathoracic pressure by controlling ventilation rate and volume; and
3. Maintain arterial pO2 and pCO2 at acceptable levels to optimize conditions for successful defibrillation and a subsequent ROSC.
As further research is conducted, providing artificial ventilations during the acute phase of resuscitation may come to be viewed as an anachronism worthy of dismissal entirely. For now, the need to maintain adequate pO2 and reduce excessive pCO2 requires us to continue to engage in a more conservative approach with respect to changing existing ventilation practices until such time as these values can be shown to have a negligible effect on the overall outcome of cardiac arrest survival. In service of this goal, we’re able to advocate incorporating upstroke ventilation into an overall new approach to cardiac arrest management in the field—one that has demonstrated a significant improvement over previous paradigms in the one metric that truly counts: discharge from definitive care without functional impairment. In doing so, we are poised to make a dramatic difference in the lives of those who matter most: our patients.
1. Sayre MR, Cantrell SA, White LJ, et al. Impact of the 2005 American Heart Association cardiopulmonary resuscitation and emergency cardiovascular care guidelines on out-of-hospital cardiac arrest survival.Prehosp Emerg Care. 2009;13(4):469–477.
2. Tang W, Weil MH, Sun S, et al. Cardiopulmonary resuscitation by precordial compression but without mechanical ventilation. Am J Respir Crit Care Med. 1994;150(6):1709–1713.
3. Noc M, Weil MH, Tang W, et al. Mechanical ventilation may not be essential for initial cardiopulmonary resuscitation. Chest.1995;108(3):821–827.
4. Bobrow BJ, Ewy GA. Ventilation during resuscitation efforts for out-of-hospital primary cardiac arrest. Curr Opin Crit Care. 2009;15(3):228–233.
5. Wenzel V, Lindner KH, Prengel AW. Ventilation during cardiopulmonary resuscitation (CPR): A literature study and analysis of ventilation strategies. Anaesthesist. 1997;46(2):133–141.
6. Kellum MJ, Kennedy KW, Ewy GA. Cardiocerebral resuscitation improves survival of patients with out-of-hospital cardiac arrest. Am J Med. 2006;119(4): 335–340.
7. Hallstrom A, Cobb L, Johnson E, et al. Cardiopulmonary resuscitation by chest compression alone or with mouth-to-mouth ventilation. N Engl J Med. 2000;342(21):1546–1553.
8. Tucker KJ, Idris AH, Wenzel V, et al. Changes in arterial and mixed venous blood gases during untreated ventricular fibrillation and cardiopulmonary resuscitation.Resuscitation. 1994;28(2):137–141.
9. Hayes MM, Ewy GA, Anavy ND, et al. Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out-of-hospital ventricular fibrillation. Resuscitation. 2007;74(2):357–365.
10. Berg RA, Kern KB, Hilwig RW, et al. Assisted ventilation does not improve outcome in a porcine model of single rescuer bystander cardiopulmonary resuscitation. Circulation. 1997;95(6):1635–1641.