M argaret Reynolds, age 57, was admitted to the ED with chest pain. (This is a real case. The patient's name and the case's details have been changed.) She was awakened at 3 AM by chest pain radiating to her left arm. The pain was accompanied by nausea and one episode of vomiting. She had no dizziness, syncope, or shortness of breath. Ms. Reynolds rated the pain at 8 on a scale of 0 to 10. She first noted pain relief after a nitroglycerin patch was applied in the ED. Her initial vital signs were blood pressure, 120/82 mmHg; temperature, 97.3[degrees]F; heart rate, 81 beats per minute; respirations, 18 breaths per minute.
Ms. Reynolds related a history of osteoarthritis, anxiety, hypertension, hypercholesterolemia, and gastroesophageal reflux disease. Before admission her medications were alprazolam (Xanax), fluoxetine (Prozac), atorvastatin (Lipitor), verapamil (Calan and others), and an unspecified codeine compound for arthritis.
She smoked one pack of cigarettes per day for 30 years. She denied using illicit drugs or alcohol.
According to Ms. Reynolds, her father had died of lung cancer at age 69. Her mother had died of myocardial infarction at age 71.
After experiencing two or three similar episodes of chest pain several years earlier, Ms. Reynolds had had exercise stress test scintigraphy; results had shown no abnormalities. Exercise stress testing is part of the process for determining the etiology of chest pain. It aids in establishing the diagnosis of coronary artery disease, determining functional capacity, and assessing prognosis.1 Ms. Reynolds had also had an electrophysiologic study several months before the present admission to evaluate recurrent palpitations and premature ventricular contractions (PVCs). An electrophysiologic study involves applying a series of programmed electrical stimuli to the heart through intracardiac catheters; it's used to evaluate various abnormal cardiac rhythms.2 In this case, it was unable to induce any PVCs or ventricular tachycardia.
Admission laboratory tests showed no cardiac enzyme abnormalities, with normal levels of troponin and creatine phosphokinase. A drug screen was positive for cocaine and opiates, in addition to benzodiazepines. All other laboratory results were within normal limits. The results of cardiolyte exercise stress testing were negative for reversible ischemia. A two-dimensional echocardiogram demonstrated normal left ventricular function, with an estimated ejection fraction of 55%.
An electrocardiogram was obtained. It is presented here for you to use in your assessment.
EVALUATING A RHYTHM STRIP
Sinus rhythm. The P wave should be upright and precede the QRS complex with a normal PR interval of between 0.12 and 0.2 seconds. That indicates that the impulse shown on the strip started in the sinoatrial node and traveled without interference through the atrium to the atrioventricular node and then to the ventricles. This is known as sinus rhythm.
The first step in evaluating a rhythm strip is to look at the overall rhythm. Is it regular or irregular? Is it generally regular with occasional abnormal beats? If so, how frequent is the irregularity? Circle any variant or ectopic beat; you'll look at it again later. For now, look at the rest of the strip.
Are the P waves regular? Does an upright P wave precede the QRS complex in every case? Measure the durations of the PR interval and the QRS complex. Horizontal movement through each small box on the rhythm strip represents 0.04 seconds. Is the PR interval between 0.12 and 0.2 seconds long (that is, does it extend over three to five small horizontal boxes?)? Is the QRS duration less than 0.12 seconds (in other words, less than three small boxes on the strip?)? Do all the QRS complexes look alike?
Calculate the rate of the rhythm. A quick method for calculating the rate is to count the number of QRS complexes in a six-second strip and multiply by 10. Another approach, which is more accurate and should be used when the strip shows irregular rhythms, is the box method. Count the number of small boxes between two consecutive QRS complexes and divide that number into 1,500.
The intrinsic rate of the sinus node is 60 to 100 beats per minute. A slower rate is called bradycardia; a faster rate is tachycardia. On Ms. Reynolds's rhythm strip, the rate is 75 to 85, right in the middle of the intrinsic sinus rate. Therefore, the strip shows sinus rhythm. There are slight variations in R-R measurements.
Next, go back and examine those unusual beats you circled. Do the ectopic beats appear early or late in the rhythm pattern? A beat that appears earlier than expected is a premature beat; if it's later, it's an escape beat. Does the QRS portion of a complex with an irregular beat appear to be the same as that of a sinus complex? That indicates that conduction is altered only above the ventricle. Is the QRS widened? In that case, the impulse originated in the ventricle or did not follow the normal conducting pathway, but rather traveled through the less conductive ventricular tissue.
In Ms. Reynolds's case, the unusual beat comes early and has no preceding P wave, and the QRS is wide-in other words, the isolated complex is a PVC. When there are multiple PVCs you must compare them; if they are identical in form they originate from the same focus. Every time the ectopic focus fires, the electric current follows the same path, resulting in complexes of identical shape.3 In addition, the T wave of a PVC often extends in the opposite direction of the QRS complex. If the PVCs don't look the same, they originate from different foci and are called multifocal PVCs.
Put the pieces together. Ms. Reynolds's rhythm strip shows normal sinus rhythm with a PVC.
TREATMENT
When PVCs are present, the possibility of underlying structural heart disease needs to be explored. Underlying heart disease influences the prognosis and therapeutic choices. Treatment of PVCs depends on their cause, the patient's symptoms, and the overall clinical picture.3
A variety of stimuli may be associated with PVCs. These irregular beats can occur with ischemia, hypoxia, or infection. They can be provoked by medications, electrolyte imbalance, cocaine use, and excessive use of tobacco, caffeine, or alcohol.3, 4
Ms. Reynolds's drug screen was positive for cocaine. The precise mechanisms by which cocaine causes cardiac arrhythmia are not clearly understood. Cocaine enhances sympathetic activation, causing vasoconstriction of coronary arteries, and increases the three major determinants of myocardial oxygen demand: heart rate, left ventricular wall tension, and left ventricular contractility. Use of cocaine may also increase ventricular irritability.5
Antihypertensive therapy can lead to regression of left ventricular hypertrophy in the hypertensive patient. [beta]-blockers have been shown to improve survival in patients with a history of myocardial infarction or heart failure.6 However, the positive drug screen means that [beta]-blockers are not the best choice to treat PVCs in this patient.7 Cocaine affects both [alpha]- and [beta]-adrenergic receptors, and treatment with a [beta]-blocker may leave the effects of [beta]-blockade unopposed, reducing coronary blood flow and worsening any myocardial ischemia already present.6
Although isolated PVCs are relatively common, they are generally asymptomatic or associated with only mild symptoms. Appropriate intervention for PVCs depends in part on whether the premature beats produce symptoms. There is no clear evidence that PVCs alone require medical intervention.
Some antiarrhythmic drugs, such as flecainide (Tambocor), actually increase the risk of death by inducing irregular rhythm, a phenomenon known as proarrhythmia.8 Therefore, treatment may pose a greater risk than the premature beats themselves do. When an antiarrhythmic drug is needed to suppress PVC-related symptoms, amiodarone (Cordarone, Pacerone) may prove effective. This medication has little potential for causing proarrhythmia.9
A small percentage of patients with drug-refractory PVCs are very symptomatic. In these patients, radiofrequency catheter ablation may be considered. One small study showed it to be effective.10 A careful risk-benefit assessment is essential before undertaking this procedure. Risks include complete heart block, thromboembolism, problems resulting from vascular access (such as bleeding, infection, and hematoma), cardiac trauma (for example, myocardial perforation), cardiac arrhythmias, pericarditis, pulmonary vein stenosis, phrenic nerve paralysis, and radiation burns to the skin.11
Other treatment options for PVCs include biofeedback, exercise, anxiolytic medications, and stress reduction. The benefits of these interventions and the influence of the placebo effect have not been clearly elucidated.9, 12
Ms. Reynolds was discharged on her preadmission medications; no treatment was ordered for the PVCs. The specific etiology of the PVCs in this case was not discovered. However, the patient's history of hypertension and hypercholesterolemia, tobacco and cocaine use, and recurrent episodes of chest pain, coupled with her family history, make it vital that she be taught about ways to improve heart health. Referrals for smoking cessation, pain management for arthritis, and counseling for illicit drug use need to be part of this patient's discharge planning.
REFERENCES