How to Approach a Narrow-Complex SVT
In general, what ultimately decides the clinical manifestations of an arrhythmia is how the ventricles are performing. In a patient who does not have significant underlying heart disease, the loss of the atrial kick can be compensated for as long as the ventricular response is controlled and the ventricles are contracting efficiently. The problem is that in SVTs the ventricular rates may not always be controlled. Typically, young, healthy individuals with no underlying cardiac disease will be able to tolerate most of the SVTs without major difficulty. However, the older patient or those with underlying coronary artery disease (CAD) or disorders may not fare as well. Prudent observation and care must be given to these patients to ensure a good outcome.
History and Physical Examination
The main purpose of obtaining a good history and physical examination early in the clinical presentation is to determine the presence or absence of hemodynamic instability. Any sign of hemodynamic instability requires emergent action to reestablish a stable, controlled rhythm with efficient and synchronized mechanical contractions of the ventricles. After hemodynamic stability is verified or achieved, the secondary goal is to diagnose the rhythm involved. Precipitating factors and the clinical course should be sought out aggressively from the patient, their families, or bystanders. Simultaneously, a rhythm strip or ECG should be obtained early and the patient placed on a monitor to evaluate the rhythm closely.
Patient history should focus on age, sex, age at onset of SVT episodes, frequency and duration of the episodes, mode of onset, triggers for onset and termination of the sensations, and past medical history of structural heart disease. Arrhythmias that involve reentry circuits are usually triggered by premature beats or the presence of precipitating factors, such as caffeine, alcohol, recreational drugs, and hyperthyroidism. A history of structural heart disease should always be sought out and can help differentiate between congenital or acquired defects (surgery, trauma, past history of CAD or AMI). Structural defects or scarring predisposes the patient to reentry tachycardias, including ventricular fibrillation in cases of wide-complex tachycardias.
Patients typically present with symptoms of palpitations, anxiety, chest pain or discomfort, pounding in the neck or chest, light-headedness, diaphoresis, and shortness of breath. Syncope is an uncommon presentation in this group, but you should always think of arrhythmias as a possible cause for any syncopal episode. Polyuria (increased urination) can also occur due to receptor-mediated increases in the levels of atrial natriuretic factor.
Palpitations are the most common presenting symptom. You should always try to determine the onset, regularity, and duration of the palpitations since they can provide strong clues as to the arrhythmia involved. Regular, sudden-onset palpitations suggest a reentrant or triggered SVT. These include AVNRT, AVRT, sinus node reentry tachycardia, junctional tachycardia, or atrial flutter. Regular, gradual-onset palpitations include atrial and junctional tachycardias with their “wind-up” onset and “cool-down” termination processes. Irregular palpitations occur in the presence of premature complexes, atrial fibrillation, or MAT.
History of prior episodes of rhythm abnormalities should always be sought out. Family history should include a thorough review of cardiac deaths occurring in younger individuals, sudden cardiac death, or arrhythmia-related symptoms or complications. Many arrhythmia disorders are linked to genetic predisposition, including diseases that prolong the QT interval (e.g., Romano-Ward syndrome, which is linked with torsade de pointes) or are associated with sudden cardiac death (e.g., Brugada syndrome).
Physical examination in a hemodynamically unstable patient will show signs of hemodynamic and respiratory compromise. The unstable patient will typically have a general appearance that reflects the lack of adequate perfusion. The patient could show signs of mental confusion or delirium, irritability or flaccidity, and possibly trauma secondary to syncope or seizure activity. The patient will exhibit pallor or cyanosis; diaphoresis; cool, clammy skin; poor capillary refill time on the nail beds; regular or irregular rapid pulse; rapid, shallow breathing with possible use of accessory muscles; poor oxygen saturation; and hypotension.
INTERMEDIATE
Physical examination in a hemodynamically stable patient can show cannon A waves and/or provide clues to a possible cardiac malformation or an underlying arrhythmia (see the Additional Information box on cannon A waves). Patients with AVNRT frequently describe a feeling of pounding in their neck or feeling their collars shake occasionally, due to the presence of cannon A waves. Cannon A waves occur when the right atrium contracts at a time when the tricuspid valve is closed. This finding is also found in patients with AV dissociation or third-degree AV block.
We encourage you to spend some time with a good book on physical examination to review the findings of a good cardiac examination. Attention to details such as clubbing of the finger and toenails; petechial, splinter hemorrhages; peripheral edema; ascites (fluid in the abdomen); and general appearance can also enhance your diagnostic acumen.
Additional Information INTERMEDIATE
Cannon A Waves
Cannon A waves are a physical examination finding that occurs intermittently, representing an abrupt and sudden elevation in the jugular venous system, caused by a transient increase in jugular venous pressure. The elevation of the jugular venous pressure occurs when the right atrium contracts prematurely against a closed tricuspid valve. Since the blood cannot move into the ventricles due to the closed valves, the blood must rush backward into the jugular and vena caval systems, leading to the formation of the large cannon A waves. This transient loss of synchronized contraction is typically due to an abnormal rhythmic event or an arrhythmia.
It is important to evaluate the signs and symptoms of SVT to distinguish them from those of panic disorders, anxiety disorders, and/or any condition that could heighten the patient’s self-awareness of a sinus tachycardia. It is common for clinicians to believe that the patient’s symptoms are due to their “irrational” behavior. Anxiety or psychological causation should be considered only once you have ruled out organic causes. Typically, clinicians learn through the school of hard knocks that psychiatric patients can have arrhythmias, too. As a matter of fact, many of the medications used to treat depression, anxiety, and psychosis have a strong history of causing rhythm disturbances.
CLINICAL PEARL
Anxiety or psychological causation for any sign, symptom, or disease should be considered only once you have ruled out organic causes.
Events do not occur in a vacuum. You need to evaluate everything together to formulate an elegant diagnosis or a comprehensive list of possible diagnoses. As we all know, our mommas are always right. That is why at a very early age, they teach us some important life lessons. One of the biggest lessons, and one we will keep repeating to you over and over, is always look at the company it keeps!