Supraventricular Tachycardi A Case Study

Supraventricular tachycardia (SVT) is a term used to describe any tachycardic heart rhythms originating above the ventricles (Ellis, 2012). This arrhythmia is caused when the either the sinus node, atrium, or the atrioventricular (AV) junction become “hyper” and fire before the next sinus beat is due. It is not possible to discern which location this premature electrical stimulus originates from because P waves are not discernable in this rhythm; however, because the QRS complex is less than 0.12 second, it can be determined the signal originates above the ventricles (Ellis, 2012). Hyperactivity resulting in a SVT rhythm may be caused by certain medications, stimulants such as caffeine, bronchodilators, tobacco products, hypoxia, or heart disease
BP uses systolic and diastolic blood pressure measures to determine the amount of force pushing against artery walls when the heart is at rest and contracting. Systolic BP (SBP) reflects the change in artery pressures related to ventricular SV (McLean, 2015). In this case study, the underlying arrhythmia for the patient was determined to be atrial fibrillation (AF). Patient’s last BP measure was 80/50. Will this new diagnosis improve the patient’s BP? Not really. While adenosine may slow the electrical conduction rate of the heart, the pathophysiology of AF still creates a problem for a normal BP. AF occurs when multiple irritable foci, potentially hundreds, from different locations across the atrium, all fire at the same time. As a result, instead of the atria contracting in one effective motion, they now depolarize in small sections. This causes the atrium to “wiggle” or fibrillate instead of contract (Ellis, 2012). Without the atrial contraction, cardiac output decreases because of the loss of the atrial kick which, according to Ellis (2012), “accounts for 15% to 30% of cardiac output.” This decrease in preload will continue to negatively affect left ventricular