It had been a bad summer for her asthma, eight attacks already. That August morning, though, it was much worse. Sitting upright with her eyes closed, she tried biting the good air and swallowing it into her lungs. But even the sounds of her wheezes were failing. She shuffled through the door of the emergency department held up by the taxi driver and then collapsed. Pulseless.
She was intubated and chest compressions were started in the next several instants. It took five minutes before her heart began beating on its own, but she was left comatose.
Bags of ice were packed around her for cooling. She had episodes of posturing during the first several hours, though she was responding to touches 18 hours after her arrest. Pupillary reflexes returned shortly after. The hypothermia was stopped at 24 hours after arrest, and she was allowed to warm slowly. She was awake and responsive 48 hours after the arrest, and she was discharged neurologically intact 11 days later.
Similar stories happen in every emergency department every day. What's amazing about this one, however, is that it was published as a case report by G. Rainey Williams and Frank Spencer in the Annals of Surgery in 1958. Yes, 1958! (Ann Surg 1958;148:462.) Despite almost 60 years between us and this case report, every element of CPR is recognizable and essentially unchanged, including our dismal ability to get the heart pumping again.
What it would it take to double the survival rate? Is it possible to triple it?
Forward flow in the aorta falls rapidly when the heart arrests, but it takes about four minutes before the pressure of the arterial and venous system equalizes and flow stops completely. The blood emptying from the arteries pools in the venous system, markedly distending the right ventricle. Carotid flow decreases similarly but more rapidly. Coronary blood flow falls even more precipitously, and then actually flows backwards for several minutes before stopping all together.
Chest compressions during cardiac arrest have only two goals. First, you must generate enough coronary blood flow to deliver oxygen to the profoundly ischemic heart. The higher the coronary perfusion pressure, the better chance we have of achieving ROSC. This is made tougher, however, because forward blood flow in the coronary arteries only occurs during the decompression phase of chest compressions (equivalent to diastole). It also takes several seconds to restore coronary blood flow after any interruptions because the pressure gradient needs to be reestablished. Brain cells become ischemic when tissue oxygen content is less than 8 mm Hg. The second goal is to deliver oxygen to the brain to prevent neurologic injury. Fortunately, cerebral perfusion occurs during systole and diastole.
Standard chest compressions typically deliver about 25 percent of normal cardiac output. We need to generate more cardiac output to improve ROSC and survival rates, and direct it as much as we can toward the heart and brain. Mechanical chest compression devices are able to provide perfect, tireless, quality chest compressions. They compress exactly to 50 mm at a perfect rate of 100. They don't lean against the patient and don't ever stop until we say so. But even so, high-quality guideline-driven chest compressions have not shown to improve ROSC or survival rates in the LINC trial among others. (JAMA 2014;311:53.)
Blood flow is dependent on refilling the heart during the decompression phase during chest compressions. Increasing venous return will deliver more blood to the heart, which can be driven forward with each compression. Passive recoil of the chest draws air into the lung and blood into the chest, but is not very effective and gets worse as rib fractures occur. We can, however, actively expand the chest during decompression by generating a larger negative intrathoracic pressure, which will reduce the right atrial pressure and draw more blood into the thoracic cavity and fill the heart. More blood will be available for cardiac output on each subsequent compression cycle. The larger negative intrathoracic pressure has the additional benefit of lower intracranial pressure, which enhances cerebral blood flow by lowering venous back flow. It is difficult to maintain large negative intrathoracic pressures with a typical airway circuit.
A check-valve type device known as an ITD (impedance threshold device) can help maintain the negative pressure, however. Air is forced out of the thoracic cavity through the device during chest compression, and the check valve closes and air is prevented from entering the thoracic cavity during decompression, which means the negative pressure can be maintained and drive venous return. Trials testing the ITD and active compression-decompression independently did not show benefit, but when used together did find a 50 percent improvement in neurologically intact survival at one year for cardiac arrest of cardiac origin in the ResQ trial. (Lancet 2011;377:301.) A confirmatory study showed a 34 percent improvement for all cardiac arrests regardless of etiology. The LUCAS device should not be considered an ACD device. It only applies three pounds of force, compared with the 20-25 pounds tested in the trials.
A mechanical device delivering chest compressions allows for possibilities that couldn't be considered before. Small elevators in Korea have been a problem for EMS personnel transporting patients, so they would transport patients with legs up attempting to increase venous return. Unfortunately, this inadvertently raised ICP and led to worse neurologic outcomes. Using a LUCAS device and ITD makes it possible to continue chest compressions in a head's up position, which is something difficult to do with manual chest compressions. The right atrial pressure is lower in this position, which increases coronary pressure and lowers ICP, which leads to more cerebral blood flow. Cardiac output would be less without the active compression-decompression and ITD to ensure adequate venous return. (Figure 1.)
Monitoring for ROSC is important to know when to stop. End-tidal CO2 is an excellent measure of cardiac output in low-flow states, such as in arrest. It measures the alveolar carbon dioxide content at the end of expiration. As long as ventilations are provided, the EtCO2 is a reflection of blood flow through the pulmonary circuit, which is the same as cardiac output. It gives a visual and effective representation of efficient chest compressions. Higher ventilation rates lower EtCO2; high-compression depth increases EtCO2. You want to target higher than 20. You see a dramatic rise in EtCO2 when the patient has ROSC. Checking pulses to differentiate PEA from ROSC is notoriously inaccurate and time-consuming, but is evident when using EtCO2. (Figure 2.)
Go forth and resuscitate.Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.