Case Study
A rapid response event was initiated by the bedside nurse for a patient who developed persistent tachycardia on telemetry. On arrival of the rapid response team, the patient was lying in bed, diaphoretic and uncomfortable. The patient was a 32-year-old male with a history of alcohol abuse, admitted to the hospital three days prior requesting alcohol detox. The patient was on a phenobarbital taper and as-needed diazepam for alcohol withdrawal symptoms. An alcohol withdrawal assessment score (Clinical Institute Withdrawal Assessment Alcohol (CIWA) score) was administered 15 min before the code was called and was 21.
Vital Signs
Temperature: 98.4 °F, axillary
Blood Pressure: 150/90 mmHg
Pulse: 179 beats per min (bpm) ( Fig. 6.1 )
Fig. 6.1
Telemetry strip showing tachycardia at 179 bpm.
Respiratory Rate: 18 breaths per min
Pulse Oximetry: 99% oxygen saturation on room air
Focused Physical Examination
The patient was a young male who appeared diaphoretic and visibly uncomfortable. He was alert, oriented, and responding to questions appropriately. Coarse tremors were present on the extension of the upper extremities. He denied difficulty breathing, palpitations, and pain. His cardiac exam showed tachycardia with normal heart sounds and no murmurs. His lung and abdominal exams were benign.
Interventions
A cardiac monitor was attached with telemetry showing narrow complex tachycardia. The patient was given lorazepam 2 mg IV because of concern for worsening alcohol withdrawal, given the elevated CIWA score. A stat 12-lead EKG was obtained, and it showed regular, narrow complex tachycardia; P waves could not be appreciated given a heart rate >150 bpm. The patient appeared to be in supraventricular tachycardia with an unknown underlying rhythm. He was asked to blow in a 10 cc syringe for 15 seconds, while simultaneously lowering his head and raising his legs. This maneuver was repeated without success. Then, 6 mg of IV adenosine followed by a 20 cc normal saline flush was given, which successfully converted the patient’s cardiac rhythm to normal sinus rhythm. Post-conversion EKG was obtained, which showed sinus rhythm at 110 bpm. Stat troponin and electrolyte levels were obtained, and potassium and magnesium were repleted intravenously. The patient was reloaded with phenobarbital, started on scheduled lorazepam doses, and remained on the medical ward with continuous telemetry monitoring.
Final Diagnosis
Supraventricular tachycardia
Supraventricular Tachycardia
Definition and Diagnosis
Tachycardia is defined as a resting heart rate >100 bpm. Supraventricular tachycardia (SVT) is a tachyarrhythmia that originates from the atrial or atrioventricular (AV) nodal tissues. It is the most common dysrhythmia in children and young, otherwise healthy patients. SVT can be classified based on the site of origin (atrium or AV node) or regularity (irregular or regular; Fig. 6.2 ).
Usually, patients are asymptomatic between episodes of tachycardia. Arrhythmia-related symptoms include palpitations, fatigue, lightheadedness, chest pain, dyspnea, anxiety, pre-syncope, or syncope. Gradual onset and gradual termination of episodes suggest sinus tachycardia. Sudden onset and abrupt termination are considered characteristics of paroxysmal arrhythmias. Most SVTs are produced through a re-entry mechanism and can be classified based on the location of re-entry.
AV Nodal Re-entry Tachycardia (AVNRT)
This is the most common form of SVT, and the re-entry circuit lies within the AV node. These are typically paroxysmal and occur spontaneously or provoked with exertion/physiologic stress, caffeine, alcohol, beta-agonists, or sympathomimetics. EKG typically shows regular, narrow complex (QRS <120 ms) tachycardia at 140-280 bpm. P waves are absent. Pseudo R waves may be seen in V1, V2, or pseudo-S waves in leads II, III, and aVF. These pseudo waves signify P waves buried in the QRS complex ( Figs. 6.3 and 6.4 ).
