Figure 1. The heart. The autorhythmic cells controlling the pace of cardiac contractions are located in the SA node. Signals generated by the SA node travel to the AV node and down the AV bundle and branches. Source: www.med.umich.edu

“Charge the paddles to 100! Clear! No response… 200! Clear!” If you’ve watched ER, Chicago Hope, or any emergency room-based television drama, that sequence probably sounds familiar to you. Cardiac resuscitation, bringing patients “back from the dead,” is a phenomenon that has pervaded nearly every aspect of our culture today. But what many don’t realize is that it can only be used in specific situations – and those television shows may have led you to think those electric paddles can save anyone’s life.

Keeping the rhythm

Cardiac arrest was once thought to be due to a spontaneous cessation of the heart during diastole, or the resting phase of the heart. It is now known to be due to a type of cardiac rhythm known as ventricular fibrillation. In order to understand the dangers of this rhythm, you must first be familiar with the way the heart works in a healthy individual.

The heart’s tissue is made up of two types of cells: autorhythmic and contractile. Autorhythmic cells set the pace for the heart’s contractions through electrical impulses, and are therefore often referred to as the heart’s pacemaker cells. Contractile cells, as their name indicates, contract (Figure 1). Together, they work to force blood through the heart and circulatory system, bringing oxygen from the lungs to every cell in the body – especially the brain.

Autorhythmic cells are situated throughout the heart, and each can send out electrical impulses at its own pace. If you were looking at a human heart and could zoom in close enough to focus on a single pacemaker cell, you would be able to see it sending its electrical messages to the cells surrounding it. Zoom out a little bit, and you would see that the contractile cells nearby, upon receiving those messages, obey the command and flex. When many contractile cells flex at once, they generate enough force to push blood through one of the heart’s four chambers (atria and ventricles).

But in order to control when and how quickly the contractile cells do their job, the autorhythmic cells need to cooperate with one another. This cooperation is found in the form of hierarchy: at one particular spot on the heart called the sinoatrial (SA) node are located many autorhythmic cells. These particular cells happen to be the ones whose electrical impulse rates are faster than any others. They work in tandem to send out a single, large impulse to the rest of the autorhythmic cells, who, one after another, pass the message along. It is like a large marching band performing at halftime of your school’s Homecoming game: The drum major stands high up on a platform to direct his or her members, and three or four assistants are situated at various points on the field so that all the sections of the band can keep in tempo. The drum major is like the SA node, directing the tempo of the beats to the other conductors, who relay the message to the band. Each band member is like a cardiac contractile cell, and their music can be equated with cardiac contractions. When the assistants follow the lead of the drum major and the band members play in symphony with each other, the result is a well-orchestrated piece of music. The same thing occurs in the heart. When the SA node’s impulses are passed through the other pacemaker cells to the contractile cells at the same pace, the cells contract at once and the heart produces one heartbeat.

But what happens if, at the Homecoming game, one of the assistants decides to stop keeping time with the drum major? Maybe he wants to conduct his own tempo, or maybe he just gets tired of looking up at that platform to make sure he’s keeping the right time. As a result, the band members following his conducting will begin to play at a different tempo than that of the rest of the band. If too many of the drum majors do this, the entire band would be playing at different speeds, and all remnants of a melody would be lost. This is analogous to ventricular fibrillation.

When a heart goes into ventricular fibrillation, it is because the signals sent out by the SA node are not being followed. At some point down the chain of command from autorhythmic cell to autorhythmic cell, the message is lost. Each individual autorhythmic cell then begins to send its own impulses, and each contractile cell listens to a different one and contracts at a different time. The result is a heart that is quivering rapidly from many small, localized contractions, but failing to produce large enough contraction to successfully force blood through its chambers (Figure 2). If it is not remedied, the victim falls into cardiac arrest and can die quickly.

Today, when a person goes into cardiac arrest, resuscitation is initiated and the person is ideally saved. To restore a normal pattern of contraction to the heart, two things are done: cardiopulmonary resuscitation (CPR) and defibrillation. Rescue workers and health care providers perform CPR by compressing the patient’s chest (and therefore the heart) to mimic the heartbeat and simultaneously blow into the patient’s mouth to continue blood and oxygen flow to the brain. Defibrillation is the use of an electric current (the paddles used so often on ER) to reset the electrical impulses running through the autorhythmic cells – it’s like the drum major blowing his whistle so shrilly that everyone stops what they’re doing and looks up at him. After a moment, he brings up his baton and order is restored. The electrical pulse stops all the heart’s contractions momentarily and resets the heart; when it restarts, the hope is that the SA node will have regained control and the other autorhythmic cells will cease to dictate their own impulses. While CPR can be performed on a heart that has stopped completely, defibrillation can only be applied if the heart is exhibiting signs of activity, as in ventricular fibrillation.

Doctors go to work

Figure 2. Cardiac contraction. Signals generated in the SA node generally follow the path shown in (A), travelling to the AV node and into the ventricles, creating a single cardiac contraction. During ventricular fibrillation (B), the SA node is bypassed and autorhythmic cells throughout the heart generate signals instructing cardiac contractile cells to contract. The result is many contractions unsynchronized, so that the heart cannot contract forcefully. Source: www.agmc.org, www.mayo.edu/cv/wwwpg_cv/ep_lab/arrthythmias.htm

Throughout the centuries physicians have recorded a few descriptions of then-drastic medical techniques for life-threatening events. Respiratory efforts are recorded first, the earliest being that of Muslim philosopher Avicenna, who reported in about the year 1000 that a cannula of gold or silver could be inserted in a person’s throat to support breathing – a technique still today called intubation. Five hundred years later, the connection between ventilation and a functional heart was noted, and in the 1700s various methods of respiratory resuscitation were utilized regularly, especially for drowning victims. Attempts at cardiac resuscitation do not appear in records until the mid-19^th century, when doctors began using chloroform as an anesthetic – it was not then known that it could lead to cardiac arrest – and surgical patients began to flounder on the operating table. The response was to immediately open the patient’s chest and massage the heart internally to restart it. By the 1880s, external compressions, which did not require the risky open-chest surgery, came into practice as well. It was not as popular as direct heart massage, however, and by the 1950s, internal cardiac chest massage was the only cardiac resuscitation technique used.

It was not until 1960 that external cardiac chest compression was “re-discovered” by three researchers at Johns Hopkins University, and reported in a paper now regarded as a landmark breakthrough. But their results were met with dissatisfaction by those who felt internal compressions were the best solution, and the debate continued for years afterward. Today, when a patient goes into cardiac arrest, the protocol is to perform closed-chest compressions first, then open-chest cardiac massage if necessary. However, studies are currently underway to determine if the risks of opening a patient’s chest can be minimized enough to make open-chest cardiac massage more feasible, since it has been shown to be the more effective method of resuscitation.