Case Study
A rapid response event was initiated by the bedside nurse for a patient who had sudden onset palpitations, followed by a pre-syncope event as the patient was walking to the restroom. Upon prompt arrival of the rapid response team, it was noted that the patient was a 45-year-old male with a history of ischemic cardiomyopathy and substance use disorder who was admitted earlier in the day after acute alcohol intoxication. At the time of admission, the patient’s drug screen was positive for cocaine, methamphetamines, and opiates.
Vital Signs
Temperature: 98.3 °F, axillary
Blood Pressure: 156/85 mmHg
Pulse: 208 beats per min (bpm) – wide complex tachycardia on telemetry (see Fig. 5.1 )
Fig. 5.1
Telemetry strip showing wide complex, monomorphic tachycardia.
Respiratory Rate: 22 breaths per min
Pulse Oximetry: 93% oxygen saturation on room air
Focused Physical Examination
The patient was a middle-aged man lying in bed in mild distress. Appropriate personal protective equipment was established, and the patient was examined. The patient was alert and oriented. He reported having an uncomfortable feeling in his chest. However, he denied any dizziness or overt chest pain. His cardiac examination showed regular tachycardia. Jugular venous distension was not appreciated, and no peripheral edema was present. His lung and abdominal exams were benign.
Interventions
Cardiac defibrillator pads were attached immediately. The monitor showed wide complex tachycardia indicating possible ventricular tachycardia (VT) vs. atrial fibrillation with aberrancy. Then, 500 cc normal saline bolus was started. Stat dose of 6 mg adenosine IV was administered without any change in heart rate. Then, 12 mg IV adenosine was administered again without any effect. Stat electrocardiogram (EKG) was obtained, which showed monomorphic wide complexes consistent with VT. As next step, 150 mg IV amiodarone was administered over 10 min, which failed to terminate the malignant rhythm. A second bolus of 150 mg IV amiodarone was administered, leading to successful cardioversion to normal sinus rhythm. EKG obtained after chemical cardioversion showed a normal QRS complex without any underlying bundle branch block. Stat troponin, electrolyte panel, including magnesium level, were obtained during the event, which were all within normal limits. A 24 h IV infusion of amiodarone was initiated, and the patient was moved to the step-down unit.
Final Diagnosis
Ventricular tachycardia
Ventricular Tachycardia
The sino-atrial node is the pacemaker of the heart. The details of the cardiac conduction system are discussed in Chapter 9 . Based on the hierarchy in the electrical conduction pathway, ventricular myocytes have the slowest firing rate (20-40 bpm), which is overridden by the much faster impulse generation of all the higher pacemakers. The impulse generated by a ventricular focus produces the classic wide QRS complex (≥120 ms), and the two ventricles are not depolarizing simultaneously. This widened QRS complex can also be seen in the presence of a bundle branch block which also means that the two ventricles are not depolarizing simultaneously.
Definition and diagnosis: Tachycardia is defined as a resting heart rate >100 bpm. Tachycardia arising from a ventricular focus is called VT. VT can be non-sustained (lasting <30 s) or sustained (lasting ≥30 s or causing hemodynamic compromise before reaching the 30 s mark). VT can be monomorphic or polymorphic ( Table 5.1 ).
| Monomorphic | Polymorphic |
|---|---|
|
|
Related posts:
Full access? Get Clinical Tree
