In a previous post, we discussed the challenges of managing patients who present with ventricular storm (VS), also known as electrical storm. Patients with VS do not sustain an organized rhythm despite medical or electrical therapy. It is understood that the catecholaminergic surge, either from the underlying disease process or iatrogenic factors, plays a significant role in the pathogenesis of VS. Medical interventions such as beta-blockers (specifically esmolol) or a stellate ganglion block can mitigate the sympathetic surge, ultimately leading to rate control and better survival rates. Limited studies show that propofol can effectively manage ventricular dysrhythmias refractory to first-line antiarrhythmic. Before we examine this closely, let’s review some of the causes of electrical storm:
In one case report, a 62-year-old male presented to the ED with generalized weakness, nausea, vomiting, palpitations, and dyspnea. He was found to have wide complex tachycardia with a rate of 205 beats per minute (BPM). A trial of amiodarone 150 mg IV infusion decreased his heart rate to 180 with no change in rhythm. However, his systolic blood pressure dropped to 80 mmHg, so the infusion was discontinued. Patient also received magnesium 2 gm IV and adenosine 6 mg followed by 12 mg without change in his rhythm. In preparation for cardioversion, the patient received propofol 100 mg (1 mg/kg) IV push with rapid onset of sedation. Before the employment of cardioversion, the patient had a sudden drop in his heart rate. A repeat EKG confirmed conversion to normal sinus rhythm (NSR) without signs of ischemia or infarct. He was then transferred to a tertiary center where he received an implantable defibrillator and was discharged home five days after the initial
Another case report discusses the case of a young woman who ingested large amounts of caffeine tablets resulting in cardiac arrest and persistent ventricular fibrillation (VF). After the return of spontaneous circulation (ROSC), her EKG showed a pattern of polymorphic ventricular premature beats, with frequent transition to VF. She was given a bolus of IV propofol, and a change in her EKG immediately reflected NSR. Continuous IV propofol was then increased to 100 mg/h (2-3 mg/kg/hr), and her cardiovascular condition improved. No further ventricular arrhythmia occurred, and she did not require additional invasive critical care support.
Obviously, we can’t draw definitive conclusions based on limited case reports like the ones above. These patients received other medications and therapies which can confound the effect of propofol. But it behooves us to appreciate the potential role of propofol in managing VS.
The ‘chill’ element
The exact mechanism of propofol in ventricular dysrhythmias is not exactly understood, but it’s thought to be related to blocking sympathetic output. In animal models, propofol has been shown to act directly on the sinoatrial node and atrioventricular conduction resulting in bradycardia. However, the same mechanism does not exist in human electrophysiological studies. Propofol’s cardiovascular effects are likely due to modulation of the autonomic nervous system. Inhibition of sympathetic activity, central vagotonic effects, and resetting of baroreflexes all result in decreased heart rate and mean arterial pressure- essential elements to control when managing patients in VS.
In my practice, if a patient presents with ventricular tachycardia and they are awake with stable blood pressure, then my first choice is an antidysrhythmic agent such as amiodarone. I usually add in magnesium as I’m investigating the reversible causes of VT. If the patient requires cardioversion, then I start with a bolus dose of propofol for sedation before they are cardioverted.
When I care for cardiac arrest patients who present in VS, I first ensure a definitive airway and minimize any interventions that exacerbate the catecholaminergic surge, such as repeated epinephrine boluses. Esmolol is my preferred beta-blockade agent for these patients, but in most ED’s, propranolol is readily available and easier to administer than esmolol. If ROSC is achieved, I quickly move to IV analgesia such as IV fentanyl boluses and deep sedation with propofol. If the patient becomes hypotensive, my first choice of pressor is phenylephrine because it won’t stimulate cardiac beta-receptors. I never discontinue the propofol drip.
- Ventricular storm is a condition that is associated with a significant catecholamine surge.
- In patients with VS, prompt identification of reversible causes and avoiding interventions that increase sympathetic output will improve mortality.
- Propofol can be a helpful adjunct in mitigating the sympathetic overdrive in patients with VS
- A single propofol bolus (1 mg/kg) may be a safe and alternative therapy for VS. If unsuccessful; then the patient is sedated and ready for cardioversion.