PROCEDURE:
The patient was connected to the monitor, and continuous ECG
recordings were made. We decided to wait for spontaneous ectopy
before proceeding with instrumentation. There was absolutely no
ectopy whatsoever at baseline. Isoproterenol then was administered
starting at 2 mcg/min and was gradually incremented to 5 mcg/min.
With that, the patient developed sinus tachycardia into the 120s as
well as shaking that became quite intense. The atenolol was stopped.
There was no ventricular ectopy during the washout of isoproterenol.
Phenylephrine bolus was then administered. The patient inadvertently
received a higher then intended (100 mcg) dose of phenylephrine. He
developed a sharp severe headache that lasted approximately 2-3
minutes. His systolic blood pressure became markedly elevated and
appeared to exceed 200 mmHg. Versed, fentanyl and IV metoprolol were
administered, and within minutes the headache subsided and his blood
pressure returned to normal.
There was no ventricular ectopy elicited in response to the
phenylephrine bolus. During 75 minutes of electrocardiographic
monitoring, there was no ventricular ectopy whatsoever. At that time
we decided not to proceed with instrumentation.
DISCUSSION: Unfortunately, ventricular ectopy was
completely quiescent today. There was not a single clinical PVC that
was seen in 75 minutes of monitoring. Given the failure of diltiazem
and a beta blocker in the past to control his palpitation, one
may consider a trial of low dose antiarrhythmic drug therapy such as
sotalol or a Class 1C agent (flecainide or propafenone). This will
be further discussed with the patient today.
IMPRESSION:
1. There was no spontaneous or inducible (with drug infusion)
ventricular ectopy to guide mapping and ablation.
2. Inadvertent administration of higher than intended dose of
phenylephrine that caused elevation of systolic blood pressure and a
transient headache. This resolved prior to the patient leaving the
electrophysiology laboratory.
The patient was connected to the monitor, and continuous ECG
recordings were made. We decided to wait for spontaneous ectopy
before proceeding with instrumentation. There was absolutely no
ectopy whatsoever at baseline. Isoproterenol then was administered
starting at 2 mcg/min and was gradually incremented to 5 mcg/min.
With that, the patient developed sinus tachycardia into the 120s as
well as shaking that became quite intense. The atenolol was stopped.
There was no ventricular ectopy during the washout of isoproterenol.
Phenylephrine bolus was then administered. The patient inadvertently
received a higher then intended (100 mcg) dose of phenylephrine. He
developed a sharp severe headache that lasted approximately 2-3
minutes. His systolic blood pressure became markedly elevated and
appeared to exceed 200 mmHg. Versed, fentanyl and IV metoprolol were
administered, and within minutes the headache subsided and his blood
pressure returned to normal.
There was no ventricular ectopy elicited in response to the
phenylephrine bolus. During 75 minutes of electrocardiographic
monitoring, there was no ventricular ectopy whatsoever. At that time
we decided not to proceed with instrumentation.
DISCUSSION: Unfortunately, ventricular ectopy was
completely quiescent today. There was not a single clinical PVC that
was seen in 75 minutes of monitoring. Given the failure of diltiazem
and a beta blocker in the past to control his palpitation, one
may consider a trial of low dose antiarrhythmic drug therapy such as
sotalol or a Class 1C agent (flecainide or propafenone). This will
be further discussed with the patient today.
IMPRESSION:
1. There was no spontaneous or inducible (with drug infusion)
ventricular ectopy to guide mapping and ablation.
2. Inadvertent administration of higher than intended dose of
phenylephrine that caused elevation of systolic blood pressure and a
transient headache. This resolved prior to the patient leaving the
electrophysiology laboratory.