You and your partner are called emergent to a private residence for a mid-6os male with abdominal pain. On arrival, the patient is sitting on the corner of his bed with obvious evidence of emesis in a trash basin next to him. He tells you that around midnight, he awoke from sleep with a burning sensation in the upper abdominal regions with accompanying nausea and vomiting. Shortly after the symptoms began, he also tells you that he took a “full-size” aspirin and some Tums with no relief. Two years ago, the patient experienced an MI with stent placement, but tells you and your partner that this “feels different” than his last MI.
- GCS of 15; A/Ox4
- Skin is dusky, moist, and cool
- Strong, regular radial pulses
- Respirations appear tachypneic, mildly labored
- Able to speak in complete sentences
- No obvious external bleeding or hematemesis in the basin
- MI with stent placement
- Chronic ETOH misuse
- BP: 174/102
- HR: 88/reg
- RR: 24bpm
- SpO2: 91% on R/A
- BGL: 192mg/dl
- Temp: 97.2° F
12-Lead obtained within five minutes of patient contact.
- Patient immediately loaded; transport started towards nearest PCI center.
- O2 @4lpm via cannula started with improvement in SpO2 to 95% noted.
- Bilateral large bore IVs established.
- 4.0mg ondansetron given for nausea/vomiting.
- No more ASA given due to patient taking a “full-size” ASA prior to arrival.
- Acquired a 15-lead with no STE noted in V4R-V6R.
- One round of 0.4mg Nitroglycerin given post 15-lead with no EKG changes.
- Patient immediately treated with Brillinta en route to the cath lab.
- Immediate stent placement with diagnosis of left dominant circumflex occlusion.
- Patient discharged back to home with cardiologist follow up.
- Were you surprised that this was a LCx occlusion instead of an RCA occlusion? Why?
- What are your thoughts of ondansetron administration during active ischemia? Is there a risk of increased QT prolongation that you believe poses a threat to the patient?