Improving the Hemodynamics of CPR

Since the evolution and proliferation of AEDs, "defibrillation" has been the resounding answer to the question, "What is the single most important action that can improve cardiac arrest survival?"

But now, following publication of 2005 American Heart Association Guidelines for CPR, we know the correct answer to that question is "timely and effective CPR." This answer is based on a growing body of scientific evidence, which confirms what many of us suspected when we repeatedly witnessed remarkable cardiac arrest success rates in areas where bystander CPR was more common.

This is not to undermine the importance of defibrillation. Defibrillation is the only modality proven to convert ventricular fibrillation/tachycardia into a perfusing rhythm, and nothing in this article implies that defibrillation should not be performed. Instead, we will explore the impact of the quality of chest compressions and timing of ventilations on the effectiveness of defibrillation.

Pathophysiology of Cardiac Arrest

During the cardiac cycle, blood is ejected from the pulmonary artery and aorta during ventricular contraction (systole), as seen in Figure 1, followed by ventricular relaxation and movement of blood from the left and right atria into the ventricles (diastole), as shown in Figure 2. During diastole, the pulmonic and aortic valves also close and the coronary arteries are perfused with oxygenated blood.

Cardiac arrest occurs when the heart ceases to eject enough blood to provide adequate perfusion to the coronary and cerebral arteries. The majority of cardiac arrests are caused by lethal arrhythmias, such as ventricular fibrillation (v-fib), ventricular tachycardia (v-tach), or a total absence of electrical activity (asystole). It is speculated that a significant number of cardiac arrests begin as v-tach with a pulse that deteriorates into v-tach without a pulse, then on to v-fib, and finally asystole as perfusion of the coronary arteries diminishes to zero. Cardiac arrest can also occur with very slow, fast or normal rhythms that, for some reason, cause the heart to contract weakly or inefficiently. We refer to this condition as pulseless electrical activity (PEA) because, despite the presence of a somewhat normal rhythm, we can't feel a pulse.

When, for whatever reason, cardiac arrest occurs, the heart muscle (myocardium) extracts as much oxygen as it can from the blood remaining in the coronary arteries and lactic acid accumulates, leading to acidosis. When we apply an AED and defibrillate the heart, we stun the myocardium and stop all electrical activity. Hopefully, one of the heart's pacemakers will then begin to fire and initiate an organized rhythm, resulting in an efficient contraction of the heart. The degree of myocardial acidosis and hypoxia determine the heart's receptiveness to defibrillation.

Elsewhere in the body during cardiac arrest, blood flow ceases and a large volume of blood accumulates in the veins of the abdomen and thorax. This venous blood has gone through the capillary network and has released only 20%-30% of its oxygen content. Therefore, once cardiac arrest occurs, there is a reservoir of oxygen-containing blood in the veins, which, while somewhat depleted of oxygen, contains significantly more oxygen and less acid than that which is stagnating in the coronary arteries.

Physiology of CPR

CPR has two components: chest compression and ventilation. Chest compression has two phases--the active phase, when force is applied downward on the chest, and the passive phase, when pressure is released and the chest is allowed to recoil to its normal shape. During the active phase, the heart is squeezed between the sternum and the spine, compressing the ventricles and causing blood to be pumped out to the lungs and body. To be effective, compression depth should be between four and five centimeters. Venous blood returns to the heart during the passive phase, flowing through the atria and into the ventricles. During cardiac arrest, venous blood will return to the heart only if the intrathoracic pressure is less than the intra-abdominal pressure. This is critical to the effectiveness of CPR.

As stated before, coronary artery perfusion occurs during the passive phase when blood ejected out of the aorta flushes back against the closed aortic valve and is diverted into the coronary arteries. Just as there needs to be a sufficient blood pressure to adequately perfuse the brain, the same is true for the coronary arteries. During cardiac arrest, it takes 5-10 efficient chest compressions to bring the coronary artery perfusion pressure up to a level adequate to supply the myocardium. Stopping chest compression even for a few moments causes the coronary perfusion pressures to drop dramatically, losing all ground made during the previous cycle of compressions. Unless coronary artery perfusion pressures can be kept consistently elevated, the hypoxia and acidosis will not be corrected.

The other component of CPR is ventilation. When we squeeze the resuscitation bag, air is forced into the lungs, providing oxygen to the pulmonary arteries and removing carbon dioxide. Because the lungs are very efficient at extracting oxygen, we now recognize that removal of carbon dioxide is the more important component of ventilation and occurs primarily through maintaining a patent airway and ensuring that a sufficient amount of air (tidal volume) is moved in and out of the lungs. The downside of ventilation is that when the lungs are inflated with air, the intrathoracic pressure rises and inhibits venous blood return to the heart.

Therefore, the keys to effective CPR are twofold:

1. Maintain adequate coronary artery perfusion by compressing the heart at the proper rate and depth.
2. Promote venous blood return to the heart by utilizing techniques to lower intrathoracic pressures.

Several studies have measured the quality of CPR performed both in and out of the hospital. They have consistently shown that we have not been doing a good job. Specifically:

• We interrupt CPR too frequently to perform other tasks, resulting, on average, in fewer than 60 compressions per minute being delivered.
• We don't compress the chest fast enough or deep enough, resulting in low coronary perfusion pressures.
• We hyperventilate our patients with high tidal volumes, which cause greater interruptions in chest compressions, but, more important, inhibit venous blood return to the heart by increasing intrathoracic pressures.
• Due to poor technique and/or rescuer fatigue, we don't allow the chest to recoil completely, leading to even higher intrathoracic pressures.

Enter the 2005 Guidelines

Based on what we now understand about the pathophysiology of cardiac arrest, physiology of CPR and the latest research, the AHA has released new CPR guidelines to address each of the issues previously discussed. They consist of the following key components:

1. Optimal compression rate is 100/minute, regardless of the number of rescuers or whether or not an advanced airway is in place.
2. Interruptions to CPR must be avoided and kept to a minimum.
3. Optimal compression depth is 4-5 cm. It is vital to relieve all pressure off the chest and allow it to completely recoil during the passive phase.
4. When one rescuer is performing CPR the ratio of compressions to ventilations is 30:2. When two rescuers are performing CPR the ratio is 30:2 for adults and 15:2 for children, until an advanced airway is in place. This results in more compressions per minute and limits hyperventilation.
5. Ventilations should be at a rate of 8-10 breaths per minute.
6. Ventilations should be given in one second; use only enough tidal volume to result in a rise in the chest wall. The second breath should coincide with the first compression in the next CPR cycle, whenever possible.
7. Once an advanced airway is in place, the ratios cease to be used and chest compressions are performed nonstop at 100/minute, with breaths delivered at a rate of 8-10/minute without pausing compressions to deliver the ventilations.
8. Unless the patient suffers a witnessed arrest and the AED is immediately available, CPR should be performed for about two minutes to "prime" the heart by raising the coronary artery perfusion pressures, washing out the hypoxic blood and improving venous blood return to the heart.

The primary goal of the new guidelines is to create the most optimal metabolic environment for the heart so that defibrillation will result in a return of spontaneous circulation.

New Techniques to Improve CPR

In addition to the new AHA guidelines, there has been substantial research supporting the use of devices that enhance the effectiveness of CPR by providing more consistent and effective chest compressions, encouraging proper ventilation rates and improving venous blood return to the heart by lowering intrathoracic pressures.

Mechanical CPR devices

Because we now know that CPR performed effectively improves cardiac arrest survival and that rescuer fatigue can significantly undermine this performance, it makes sense to consider taking the human out of the equation. Several companies have brought forth devices to do just that, and there is data to support their use, not only from a patient survival perspective, but from an effective use of rescuer manpower.

The AutoPulse (Figure 3) from ZOLL Medical, utilizes a constricting band that is pneumatically controlled and compresses the chest automatically using a built-in electronic control. AED pads can be placed under the band and defibrillation delivered with minimal interruption in chest compressions. Studies have shown that the AutoPulse generates better blood pressures and cardiac output than conventional manual CPR.

The Thumper (Figure 4), a pneumatic compression device, has been on the market for many years. Despite the lack of recent research regarding its effectiveness, the mechanics involved appear to be consistent with the goals for effective CPR.

Devices designed to decrease intrathoracic pressure

Both the AutoPulse and the Thumper utilize only active compression of the chest, allowing it to recoil passively. Another form of CPR is called active compression/decompression CPR (ACD-CPR), during which the device not only actively compresses the chest, but, by way of an adhesive pad attached to the chest, actively pulls upward, expanding the chest during the relaxation phase. The advantage of such a device is that it significantly decreases the intrathoracic pressure, which, as discussed before, improves venous blood return to the heart. Unfortunately, the FDA has yet to approve such a device in the United States. In the United Kingdom and elsewhere, a device called LUCAS is used to perform ACD-CPR. A study is currently being performed in the U.S. on a manual ACD-CPR device called the ResQPump (see Figure 5). It will be interesting to learn whether a manual ACD-CPR device can replicate the performance of the automatic device.

Since ventilation significantly increases intrathoracic pressure, our goal must be to limit it to a rate and volume sufficient for gas exchange. When the chest is compressed, air is forced out. The lungs refill with air during the recoil phase, even when the resuscitation bag is not squeezed. This "inhaled" air increases intrathoracic pressure. If these unnecessary respiratory gases could be prevented from entering the chest, the intrathoracic pressures could be significantly lowered. The inspiratory impedance threshold device (ITD) does just that. The only ITD currently on the market is the ResQPod (see Figure 6), manufactured by Advanced Circulatory Systems, which also makes the ResQPump.

The device can be used with a conventional mask, but requires that the mask-face seal be maintained continuously so as not to allow air to passively enter the chest. Once an advanced airway is inserted, the ResQPod is attached and the resuscitation bag is attached to the ResQPod. When the chest is compressed, the air in the lungs is forced out the advanced airway and through the ResQPod. During chest recoil, passive inflow of air is prevented, resulting in a negative intrathoracic pressure. The device does not interfere with ventilation, allowing the rescuer to squeeze the resuscitation bag and deliver air to the lungs. Another helpful feature of the device is a set of LED timing lights that blink at a rate of 10 times per minute. When the light flashes, the resuscitation bag is squeezed, further ensuring that the patient is not hyperventilated.

CPR performed using the ResQPod results in significant elevation of both coronary and cerebral artery perfusion pressures as a result of the lowered intrathoracic pressure, which promotes greater venous blood return to the heart. These elevated perfusion pressures and cardiac output enhance oxygenation of the heart. Studies using the ResQPod have demonstrated significant improvement in return of spontaneous circulation and survival to the hospital, particularly for patients in asystole and PEA--a group of cardiac arrest victims for whom survival has been generally considered rare.

Automated prompts

A key limitation to manual CPR appears to be the lack of controls or prompts to encourage rescuers to perform compressions and ventilations at the correct rate and depth. If manpower were no issue, wouldn't it be nice to have your AHA instructor stand behind you and measure your performance and coach you when needed? That isn't practical; however, we use manikins during training that do just that. Philips, in combination with Laerdal, has developed an integrated CPR monitoring device into its monitor/defibrillator called Q-CPR (see Figure 7). Q-CPR is a device that is attached to the patient's chest with an adhesive pad, and chest compressions are performed on top of the device (see Figure 8), which measures the rate and depth of compressions. Ventilation rate and tidal volume are measured by changes in the resistance across the chest through the ECG electrodes. This information is fed into the monitor, which then provides both auditory and visual prompts regarding the quality of CPR. When the rate of compressions falls outside the preset rates and depth, the monitor says "compress faster," "compress slower," "compress harder," etc. All of this information is stored in the monitor and can be printed out for later use in quality improvement.

ZOLL has incorporated similar technology into its AED Plus and AED Pro devices, known as Real CPR Help, which provides feedback on the rate and depth of compressions (Figure 9). Studies demonstrate that the use of voice prompts improves the quality of CPR primarily by preventing degradation of performance over the course of the resuscitation.

Summary

More research is needed to improve our understanding of what constitutes the most effective method of cardiopulmonary resuscitation; however, we know more now than ever in the history of medicine. We know that CPR is more than simply pushing on the chest and defibrillating the heart. We know that there exists an optimal physiologic condition to facilitate successful resuscitation that relies on quality coronary and cerebral artery perfusion and preparation of the heart before defibrillation.

There are many questions yet to be answered, such as how long defibrillation should be delayed following CPR, which devices or techniques provide the most effective CPR, and what are the most effective ratios of compression and ventilation?

The answer may lie within a combination of approaches using multiple devices and techniques simultaneously in an attempt to meet the goals for performing the most effective CPR.

What is clear is that the science of cardiac arrest is maturing, and what began in the early ages as an act of faith and desperation has now become grounded in logical reason and understanding of the physiology of cardiac arrest and the hemodynamics of CPR.

Bibiliography
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A. Keith Wesley, MD, FACEP, is an emergency medicine physician at St. John's Hospital in St. Paul, MN, and lives in Eau Claire, WI, with his wife, Karen, and their white lab, Dixie. He is a member of the Wisconsin EMS Section's EMS Advisory Board, the author of Fast and Easy ECGs, and a popular speaker at state and national EMS conferences.