Arrhythmias cannot be interpreted in a vacuum. We need to start off this discussion with a very simple but often overlooked fact: You need to look at, touch, and listen to your patient. When you first approach any rhythm strip, it is critical to know from whom the strip was obtained and the clinical scenario in which it was obtained. If you notice anything unusual about the rhythm, you need to physically take a look at the patient and evaluate his or her condition (or you need to inform whoever is responsible for the patient). Why? Because you can never assume that an arrhythmia is not dangerous!
Suppose you have been given a strip of a patient in ventricular bigeminy. Bigeminy is easy to diagnose and is fairly evident on the strip. You make the call and you are happy with yourself. The patient will be OK . . . ventricular bigeminy is usually a benign rhythm. The key word, however, is “usually.” The problem is that this patient did not know that she had a benign rhythm. Instead, she had no functional mechanical contraction with the premature ventricular contractions (PVCs). The bigeminal episode was actually only perfusing her body at a pulse rate of 30 beats per minute (BPM). The patient was in cardiogenic shock and needed immediate attention in order to prevent death or, at the very least, a serious complication.
As we mentioned before, we have purposely avoided treatment strategies in this text. The reason is that we wanted the text to be useful for longer than one or two years. The principles involved in arrhythmia interpretation have remained fairly stable over the years, although treatment has not. Modern medicine is changing at such a pace that most books are outdated by the time they are published. Emergent management of any hemodynamically unstable arrhythmia should be based on the American Heart Association’s Advanced Cardiac Life Support program, or any other qualified protocols that are directed toward the management of these patients. Treatment of hemodynamically stable arrhythmias can be looked up in any book that is updated yearly, on the Internet, or on any other recently updated medium, in order to make sure that you are dealing with the latest and most up-to-date information.
If your patient is in any way hemodynamically unstable, he or she needs emergent treatment. Do not wait until matters get worse. Sometimes, the patient will show only minimal signs of instability—for example, he or she will be light-headed and sweaty, with blood pressure lowered a little bit—and the next minute, he or she will have completely deteriorated. Early prevention and treatment (including defibrillation and cardioversion) may prevent a catastrophe. Remember that it takes time to get together all of the equipment and drugs that you will need to handle an emergency. Don’t wait until the problem has completely deteriorated before you start to act.
This text cannot possibly cover all of the important points about a patient’s history that could shed light on your interpretation. So, we will cover only a few important points. The key to a good history and physical exam is to be thorough and methodical. You need to have a Sherlock Holmes-like approach to your patient’s story. Nothing should be overlooked. It is usually the little things that add the most information.
To begin, for most patients, the history is the most important part of any patient evaluation. The history should include past and present information that would be pertinent to narrow your differential diagnosis. You should start by focusing your attention to the immediate incident. What was the first thing that the patient felt? In what order did the signs and symptoms present? How severe were the symptoms? How long did the symptoms last? What was the patient feeling or doing immediately before having the first symptoms? Did she pass out? Have shortness of breath? Chest pain or discomfort of any kind? Light-headedness? Sweating? Did the pain or discomfort radiate anywhere? Did she have any palpitations? How fast were the palpitations? How regular were the palpitations? (It is a good idea to have the patient tap out the palpitations on her leg or other surface. In this way, you develop a feel for the regularity and speed of the palpitations.) Was she exposed to any toxins or allergens? Did they use any street drugs? Does she smoke? These are just a few of the questions that you should think about when you approach a patient.
Past information could include past events, for example, previous episodes of tachycardia or syncope. It should also cover predisposing conditions that could be proarrhythmic. For example, a history of a previous myocardial infarction or congestive heart failure may raise your suspicions for ventricular tachycardia (VTach)as a cause of palpitations and syncope. Chronic or acute renal failure should raise the suspicion of an electrolyte abnormality that can cause some serious arrhythmias. Chronic obstructive pulmonary disease can raise your suspicion for multifocal atrial tachycardia. Leg swelling after a car trip could raise your suspicion for a pulmonary embolus and the resultant arrhythmic complications of such an event. The possibilities are endless. Every case is unique and you need to have a high index of suspicion as you approach your patient.
The family history is very important in the evaluation of many of the arrhythmias. The family history should focus on various possibilities: any family members who died suddenly at a young age or a family history of a first-degree relative who had a heart attack before the age of 55 years for males (e.g., father, brother) or before the age of 65 years for females (e.g., mother, sister).
The medications that the patient is taking can definitely shed some light on the evaluation of an arrhythmia. Many antiarrhythmics can actually increase the occurrence of life-threatening arrhythmias. There are many medications that can prolong the QT interval, including some antinausea and antiemetic medicines. Many medicines can cause gastrointestinal bleeding, renal complications, or hepatic complications that can, in turn, cause electrolyte abnormalities. Medications can bring to the surface certain previously undiagnosed genetic diseases or enzyme abnormalities. Finally, many medications can cause drug–drug interactions that cause untoward arrhythmic side effects.
Don’t be afraid to ask questions of your patients. You are not wasting time or boring them. Trust me, they want to get to the bottom of their problem. If you cannot obtain the history from them, turn to the family members or friends who are with the patient. Many times they can provide information that your patient is embarrassed to bring up. If your patient cannot remember his medications, call the house and have someone go to the medicine cabinet. All in all, don’t be afraid to use all of the resources you have available to you to come up with an answer.
The first thing to look for on the physical examination is the vital signs. The pulse rate is the physical representation of the mechanical contraction caused by the underlying heart rate and rhythm. Many times, however, the pulse rate and the rate on the monitor do not match because the electrical events do not cause a mechanical contraction or an effective mechanical contraction. Always make it a habit to double-check the monitor rate and the pulse.
Besides the simple mechanical rate, the pulse can tell you whether an arrhythmia is having an effect on organ perfusion. Weak, thready pulses are usually associated with lower states of cardiac output. Cold, clammy skin is also a sign of vascular underperfusion of the skin. The capillary refill is obtained by pushing down on the nail until the nail bed turns white. The pressure is then released and the number of seconds it takes for the normal pink color to return is measured. Capillary refill should be less than 2 seconds in the normal patient.
The pulse rate can also tell you a lot about the regularity of the rhythm. It is easy to spot the different cadences (regular, regularly irregular, or irregularly irregular) by taking the pulse. Events, such as premature contractions, can be picked up on the pulse. Unfortunately, it is not possible to tell the difference between premature atrial contractions (PACs), premature junctional contractions (PJCs), and PVCs by palpating the pulse.
The next thing to evaluate from the vital signs is the blood pressure. Most patients with significant arrhythmias, either tachyarrhythmias or bradyarrhythmias, will have some alteration in their blood pressure. The loss of atrial kick will often affect the blood pressure by altering the ejection fraction of the ventricles.
Simple gross observation of the patient can give you a quick idea about the cardiovascular status. If the patient is in extremis (looks seriously ill), it is very obvious. Patients will be diaphoretic and tachypneic, and they will usually have a look of panic or impending doom on their faces. Many times, patients will be cyanotic with a purplish discoloration to their faces. (Clinical pearl: True cyanosis, caused by low oxygen levels, will result in central cyanosis, which means that the nose and central body also appear purplish. Many rheumatologic diseases can cause peripheral cyanosis, which is caused by a clamping down of the peripheral blood vessels.)
The jugular venous waves can also provide a very significant clue to an underlying arrhythmia. An interesting physical exam finding occurs when the patient is in atrioventricular (AV) dissociation. Since the atria and ventricles are contracting at their own separate pace, the atria eventually have to contract while the AV valves are still shut. In these cases, the blood being pumped by the atria has to go somewhere. That somewhere is back up through the neck veins. The sudden pressure and volume wave caused by the atrial contraction will cause a sudden, very large, venous pulsation to develop. That very large pulsation is known as a cannon A wave. Cannon A waves can also be seen in any other rhythm that may intrinsically have AV dissociation (idioventricular, accelerated idioventricular, and VTach).
The physical exam can also provide basic clues to underlying disease processes that are associated with rhythm disturbances. Congestive heart failure, cardiomyopathies, myocardial infarctions, congenital heart disease, Down syndrome, Marfan syndrome, and the arteriovenous shunts used in chronic renal failure patients are just a few examples of these disease states.
Here is another little clinical pearl: Suppose you are asked to see a patient with unexplained syncope and a big laceration on her face which she received during the fall. Did that patient more likely lose consciousness because of a cardiac event or have a seizure? Think about it this way: An arrhythmia will cause a fast, but not instantaneous, loss of consciousness. Patients usually remember the floor coming at them as they fall and they have enough time to put their hands out to stop their faces from striking the ground. A laceration can still occur if they hit something along the way, but the chances are less likely with this type of loss of consciousness. When you have a seizure, the neurologic event is instantaneous and you lose immediate control over your body. This immediate loss of control gives you a much greater chance of hitting the ground hard with a seizure.