Practical Electrophysiology
Second Edition
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TODD J. COHEN, MD

Chapter 1 - The History of Electrophysiology

In 1895, Willem Einthoven described the waves recorded from his invention, the string galvanometer. His PQRST diagram is remarkably similar to the P, QRS, and T waves currently used daily by cardiologists everywhere for interpretation of a standard electrocardiogram (ECG). Therefore, it may appear that little has changed with respect to the image, principles, and nomenclature of a standard ECG tracing over the past century. However, tremendous changes have been made in the method of ECG recordings. For instance, there is no longer a need to immerse limbs in saline; precordial and unipolar electrodes have been developed, and digital/computerized recording systems have been implemented. Similar advancements have also been made in our understanding of electrical signals recorded from within the heart (intracardiac recordings) since the recording of the first His bundle. During the past half-century, we have witnessed the development of cardiopulmonary resuscitation, transthoracic cardioversion and defibrillation, and the advent of implantable devices (pacemakers, defibrillators, loop recorders, and biventricular devices). Innovations in catheter ablation have resulted in a very high success rate for most reentrant and focal supraventricular tachycardias and certain ventricular tachycardias. Even atrial fibrillation can be successfully managed in many circumstances via pulmonary vein isolation procedures and left atrial ablations. These procedures can be performed percutaneously with an ablation catheter.

In 1884, the first graphic documentation of ventricular fibrillation was performed by M. Hoffa. Shortly thereafter, in 1888, Augustus Desiré Waller introduced his findings on electromotive properties of the human heart. Waller presented his dog with each paw in a pan of saline, from which the electrical potentials were recorded, and termed these electrical currents “electrograms.” John A. McWilliam published his findings, “Electrical Stimulation of the Heart in Man,” in 1889; in them he stated that “in certain forms of cardiac arrest there appears to be a possibility of restoring by artificial means the rhythmic beat.”

Chapter 3 - The Cardiac Action Potential

The cardiac action potential is the recording of the changes of electrical potential over time recorded from inside a cardiac myocyte (heart muscle cell). The action potential is due to the flow of electrolytes through the plasma membrane changing the voltage across the cell. The inside of the myocyte changes its electrical potential with the inflow and outflow of electrolytes through ion channels. These ion channels serve as gates that open and close, thereby controlling the ionic flow. The gates respond to changes in the membrane potential (differences in voltage).

The potassium, sodium and calcium channels are ion channels that allow for inscription of the action potential. The potassium channels have a single voltage-sensitive gate that is closed in the resting state and opens slowly in response to depolarization. The sodium channels have two voltage-sensitive gates: a gate that is closed in the resting state and opens quickly in response to depolarization, and a gate that is open in the resting state, called the “inactivation gate”, which closes slowly in response to depolarization. As the cell is depolarized, threshold for opening the L-type calcium (Ca++) channel is achieved, which is responsible for the plateau of the action potential. When a certain threshold potential is reached, the potassium ions (K+) dribble out of the cell, while the sodium ions (Na+) pour into the cell, which causes the rapid influx of Na+ relative to the efflux of K+. The result, an increase in voltage by about 15 millivolts (mV) to 20 mV, is called the overshoot of the action potential. Figure 3.1 shows a simplistic schematic of a myocyte and its ionic channels (only Na+ and K+ illustrated).

Chapter 6 - The Electrophysiology Laboratory

 The electrophysiology laboratory is a unique place for the diagnosis and treatment of cardiac arrhythmias. In general, it is an invasive laboratory very similar to the cardiac catheterization laboratory. The laboratory should be electrically isolated (free of outside electrical noise), since in addition to recording standard body surface electrocardiograms, high-fidelity intracardiac electrograms (recordings from inside the myocardium) are recorded.

The lab contains a fluoroscopy table that in some cases may be able to tilt the head upward as well as downward (as in the Trendelenburg position, in which the feet are raised above the head to help pool venous blood back into the central circulation). The tilting motion may be helpful in gaining access to the blood vessels in order to insert catheter and/or introducer sheaths. It is also helpful if the patient has low blood pressure. In some laboratories, the table can tilt upward at least 60 degrees to facilitate head-up tilt-table testing (the procedure to diagnose vasovagal syncope or neurocardiogenic syncope). This table should be able to tilt rapidly up and down, and it should be stable enough to accommodate the weight of the patient.

Chapter 8 - Venous and Arterial Access

In the beginning of an electrophysiology study, it is important to gain venous and/or arterial access. This is essentially placing an intravenous catheter (an introducer sheath) into a vein and/or artery. For electrophysiology procedures, it is not uncommon to place three introducer sheaths into a single femoral vein.

First, the femoral artery and/or vein must be located so that the operator can access the circulation in order to perform an electrophysiology study. The operator can identify the appropriate location by palpating the groin area of the patient near the iliac crest and the ischial tuberosity, as well as the symphysis pubis.

The inguinal ligament extends from the iliac crest down to the symphysis pubis. About two-thirds of the way medial between this location, one should be able to palpate the femoral artery, below the femoral ligament. There is a triangle in which the femoral nerve, artery, and vein are located from lateral to medial (figure 8.1). By using the mnemonic NAVel, you can remember that the nerve, the artery, and the vein are always facing the navel whether one proceeds from the right or left side. In other words, the nerve (N) is most lateral, followed by the artery (A), and then the vein (V) as the most medial of the structures.


Chapter 15 - Atrial Fibrillation

Atrial fibrillation is one of the most common arrhythmias. According to the American Heart Association, approximately 2.2 million people in the United States are living with atrial fibrillation. The most commonly associated cardiac condition of this arrhythmia is hypertension, although it is also common to find atrial fibrillation in patients with other types of cardiac abnormalities such as myocardial infarction and ischemia, valvular disease, and hypertrophic cardiomyopathy.

Atrial fibrillation is diagnosed as an irregular rhythm in which the atrial depolarization occurs in a very fast, chaotic manner (figure 15.1). The mechanism may be related to abnormal stretch and/or foci in the myocardium at areas such as the pulmonary veins, the coronary sinus, and the right atrial appendage.

Atrial fibrillation may be classified based on two criteria: 1) episode frequency; and 2) the ability to convert spontaneously back into normal sinus rhythm. If a patient presents with two or more episodes, this is called recurrent atrial fibrillation. Recurrent atrial fibrillation may be paroxysmal (terminates spontaneously) or persistent (does not terminate spontaneously, but only after pharmacologic or electrical cardioversion). Long-standing persistent atrial fibrillation may also be called chronic atrial fibrillation. When this tachyarrhythmia is unable to be cardioverted successfully, it is called permanent atrial fibrillation.

Chapter 18 - Atrial Flutter

Typical atrial flutter is a macro-reentrant tachycardia. It differs from an atrial tachycardia (which emanates from a discrete focus) by its continuous electrical activity around a relatively large anatomic structure, such as the right tricuspid valve. It is principally a right atrial disease, but can occasionally occur in the left atrium or around surgical scars. Classic atrial flutter most frequently moves counterclockwise around the right atrial structures, but occasionally may move clockwise. Figure 18.1 shows a 12-lead ECG in a patient with typical atrial flutter. Note the sawtooth flutter waves seen in the inferior leads (II, III, and aVF).

To diagnose atrial flutter and its mechanism, it is useful to position a multipolar electrode catheter from the femoral vein and cross the isthmus into the coronary sinus. This can be seen in figure 18.2. The catheter traverses the isthmus and records continuous atrial conduction, as observed in the figure at an atrial cycle length of 259 msec. One can pace directly on the isthmus in a critical zone of the tachycardia and entrain (get into the circuit of) the tachycardia. Typically, a large (10-mm) ablation tip catheter is placed across the tricuspid valve in order to record a large ventricular electrogram with a small atrial electrogram. In the left anterior oblique fluoroscopic projection at approximately 45 degrees, the tricuspid valve is open and resembles a clock facing right at the operator (figure 18.3). The ablation is performed from that viewpoint, and the catheter tip serves as the small hand of the clock for location purposes. The operator typically performs a cavotricuspid isthmus ablation with the catheter at 6 o’clock, as viewed in the left anterior oblique projection. The author typically delivers 45 seconds of radiofrequency energy at 100 watts and a temperature of 55 degrees centigrade. Other operators may have subtle variations of the precise power, temperature, and duration of the particular radiofrequency energy applications.

Chapter 23 - Syncope

Syncope (or loss of consciousness) is one of the most frequent emergency room and hospital diagnoses. Three to six percent of hospital admissions and/or emergency room visits can be attributed to syncope or near-syncope. The workup should follow a simple algorithm. The method of evaluating syncope and determining its etiology should initially consist of a history, physical examination, and 12-lead electrocardiogram. Table 23.1 shows the common causes of syncope. Table 23.2 shows the clinical characteristics of cardiac and noncardiac syncope. Cardiac syncope primarily consists of arrhythmias of all types: tachycardias (rapid heart rhythms) such as ventricular tachycardia/fibrillation and/or supraventricular tachycardia, and bradyarrhythmias such as heart block, sinus bradycardia, and asystole. If the history, physical examination, and/or electrocardiogram point to a cardiac diagnosis, a cardiac workup may be important, followed by an electrophysiology study.

The electrophysiology study is useful at assessing cardiac conduction and presence of arrhythmias. The results of the study can focus the treatment to drugs, catheter ablation (performed at the time of the electrophysiology study), and device-based therapy (pacemaker or implantable defibrillator).

The most common etiologies of syncope are of a noncardiac vascular nature, with neurocardiogenic syncope and orthostatic hypotension accounting for approximately half of all cases. Figure 23.1 shows a schematic of the mechanism of neurocardiogenic syncope. In neurocardiogenic syncope, there is a brain-heart interaction such that a catecholamine trigger (adrenaline) causes the heart to beat forcefully (hypercontractile), thereby activating mechanoreceptor C fibers on the posterior left ventricle. Stimulation of these fibers may trigger a hyperactive vagal response with resultant bradycardia and/or hypotension. There are two types of neurocardiogenic syncope responses: a cardioinhibitory response, which is principally bradycardia-driven hypotension, and vasodepressor syncope, in which vasodilatation of the blood vessel is the primary response. In a significant number of patients with neurocardiogenic syncope, a mixed vasodepressor and cardioinhibitory response occurs.



Chapter 29 - Intravenous Drug Administration/ Preoperative Checklist

The responsibility for the administration of intravenous (IV) drugs in the EP lab lies with the nurse, under the direction of the physician. Because IV medications are delivered directly into the bloodstream, their dispensation requires more knowledge and greater precautions than do other methods of drug administration. Drug serum levels reach higher concentrations, and adverse reactions occur more rapidly and are usually more severe with the use of IV medications. Therefore, it is important to recognize the problems associated with IV drug administration and to impose caution when dispensing drugs by IV push.

IV administration ensures prompt onset of action and reduces ambiguity allied with the incompleteness of drug absorption by other routes. IV administration requires regular monitoring by a nurse, because this route increases the risk of side effects or toxicity.

It is important for the EP nurse to display an understanding of the drug to be administered by exhibiting knowledge regarding the rationale for the use of a specific drug in a particular patient, the rate of the drug administration, the drug’s possible side effects, the drug’s normal dosage range, and the compatibilities and incompatibilities of the drug with other IV drugs and fluids.
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