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63. Electrical Storm of the Heart: A Shocking Experience!
Keywords
Emergency physiciansThe diagnosisTreatmentManagementUnstable ventricular dysrhythmiasCase
Palpitations, Syncope, Recurrent VT
Pertinent History
A 47-year-old female is brought in to the emergency department by EMS. The paramedics report that the patient was found unresponsive at a high school basketball game where she was a spectator. Witnesses did not report any seizure-like activity. She awoke without any post-event confusion. Her blood glucose was 113. During transport, the cardiac monitor showed frequent runs of nonsustained ventricular tachycardia (VT). As she arrives, she is connected to your monitor and has a run of polymorphic VT for approximately 30 seconds during which time she reports feeling “light-headed” with palpations, shortness of breath (SOB), and diffuse chest discomfort. The patient is alert, oriented, and able to provide some additional history. She does not recall any prodromal symptoms prior to the event. She recalls that for the past three days she has been feeling extremely fatigued and has had episodes of palpitations with shortness of breath. Thinking back further, she has noted increased lower extremity edema over the past 1–2 weeks and was recently started on furosemide for “lower extremity edema.”
Pertinent Physical Exam
BP 97/62. HR 104, Temp 98.9F, RR 22. SpO2 94% on 4 L NC.
General: Somewhat pale, diaphoretic. Alert and oriented.
Cardiovascular: Jugular venous distension (JVD) appreciated to the level of the thyroid cartilage while sitting upright. Regular rate and rhythm during exam. +S3. Pitting edema of lower extremities to upper tibias. Lower extremities cool to touch.
Pulmonary: No apparent respiratory distress, trachea midline, posterior auscultation with crackles up to the mid-thorax bilaterally.
Abdomen: Soft, nondistended, nontender to palpation.
Past Medical History (PMH)
Hypertension, Hyperlipidemia, Type II DM, Chronic Kidney Disease Stage III.
Social History (SH)
Former smoker (~ 10 pack-years), occasional ETOH use, denies illicit substance use.
Family History (FH)
Family history notable for “enlarged heart” in her brother and father, with early cardiac death of her father at age 50. Her brother has “some kind of pacemaker.”
Pertinent Test Results
Test | Result | Units | Normal range |
|---|---|---|---|
WBC | 11.3 ↑ | K/uL | 3.8–11.0 103/ mm3 |
Hgb | 8.4 ↓ | g/dL | Male: 14–18 g/dL |
Female: 11–16 g/dL | |||
Platelets | 400 | K/uL | 140–450 K/uL |
Potassium | 3.4 ↓ | mEq/L | 3.5–5.5 mEq/L |
Magnesium | 1.6 | mg/dL | 1.6–2.6 mg/dL |
Creatinine | 2.1 ↑ | mg/dL | 0.6–1.5 mg/dL |
Lactate | 3.1 ↑ | mmol/L | < 2.0 mmol/L |
Troponin | 1.3 ↑ | ng/Ml | < 0.11 ng/mL |
BNP | 12580 ↑ | pg/ml | <100 pg/ml |
EKG
Sinus rhythm with frequent PVCs, left axis deviation, nonspecific T-wave inversions. QTc read as 457.
Chest X-ray (CXR)
Cardiomegaly, bilateral airspace disease consistent with pneumonia vs pulmonary edema. Small bilateral pleural effusions.
ED Management
There was concern for syncope secondary to primary dysrhythmia (VT/ventricular fibrillation (VF)) with new decompensated heart failure. Acute coronary syndrome was considered, and the patient was given 324 ASA, with serial troponins ordered. The admission order was placed to the cardiology service.
Updates on ED Course
Update 1 (1910)
Repeat EKG remains stable from prior.
The case was discussed with cardiology who recommended a 150 mg amiodarone bolus followed by a drip, but declined catheterization lab activation.
40 mg PO potassium was ordered as well as 4g IV magnesium.
Update 2 (1950)
A loading dose of lidocaine 1 mg/kg was ordered.
Due to declining mentation, the patient was intubated for airway protection.
Update 3 (2011)
Initial rhythm was consistent with coarse ventricular fibrillation (VF), defibrillation was attempted at 360 J unsuccessfully. The patient was given 1 mg epinephrine IV, and compressions were resumed.
At the next rhythm check, the patient reamined in VF, and defibrillation was unsuccessful at 360J. The patient was given 300 mg amiodarone IVP, and compressions were resumed.
The patient remained in VF at subsequent 2 pulse/rhythm checks.
A second external defibrillator was brought to the resuscitation room, and a second set of pads were placed in the anterior-posterior (A-P) orientation on the patient’s chest. At the next rhythm check with persistent VF, both external defibrillators were fired simultaneously at 360 J. No immediate change was noted to the rhythm.
Dual-sequence defibrillation was repeated at the next rhythm check with apparent conversion to sinus tachycardia, achieving return of spontaneous circulation (ROSC).
Postarrest EKG showed inferior ST depressions, cardiology was called, and the catheterization lab was activated.
Left heart catheterization showed mild luminal irregularities and an ejection fraction (EF) <15% by ventriculogram. Therefore, an intra-aortic balloon pump was placed.
The patient was admitted to the Coronary Care Unity for further management and propranolol 40 mg q6 was added to her medication regimen.
Learning Points: Electrical Storm
Priming Questions
- 1.
Describe some of the common mechanisms by which ventricular dysrhythmias originate.
- 2.
What criteria are used to diagnose electrical storm in patients with and without an implantable cardioverter defibrillator (ICD)?
- 3.
Outside of anti-arrhythmic medications, what pharmacologic and nonpharmacologic therapies exists for treatment of electrical storm?
Introduction/Background
- 1.
For emergency physicians, the diagnosis, treatment, and management of unstable ventricular dysrhythmias are rather simple. These patients are dead or dying. They fall quite neatly into the ACLS algorithms which are firmly engrained in our resuscitative minds. However, those patients who are “stable-ish” are at risk for devolving into electrical anarchy and may continue to require repeated therapies (electrical or pharmacologic) for their symptomatic ventricular dysrhythmias. This can be a challenging patient population to manage.
- 2.
Electrical storm is the proper term for a syndrome characterized by persistent or refractory ventricular dysrhythmias. Most commonly, this is ventricular tachycardia; hence, this entity is most frequently encountered and described as “VT storm.”
Review of multiple retrospective studies suggests that monomorphic VT accounts for 86–97% of electrical storms, with VF accounting for 1–21%. There are varying incidence of mixed VT/VF and polymorphic VT [1].
- 3.
The incidence of this syndrome is unclear. However, since the widespread implementation of ICDs, there has been perhaps a greater identification of patients with recurrent ventricular dysrhythmias as recorded on interrogation of these devices as well as the therapies that are then delivered as a result. Admittedly, these are patients with known cardiac disease; therefore, the application of this data to the general public is unclear.
For patients with ICDs placed for primary prevention (i.e., ejection fraction (EF) <35% despite revascularization and guideline-directed medical therapy), the incidence of electrical storm has been reported to be anywhere from 1.5 to 6.1%/year.
Not surprisingly, when you look at patients who had ICDs placed for secondary prevention of ventricular dysrhythmias, the incidence of electrical storm increases to upwards of 8%/year [2].
Physiology/Pathophysiology
- 1.
With regard to the pathogenesis of a particular ventricular dysrhythmia, there are three basic mechanisms by which such a rhythm is generated. This includes the following [3]:
Abnormal automaticity: Often seen in the acute phase of myocardial ischemia due to changes in membrane potential, it results in the spontaneous depolarization of ventricular myocytes or Purkinje fibers.
Triggered activity/afterdepolarizations: This occurs when another depolarization takes place at an inappropriate time during the cycle of a myocytes action potential, often seen when the action potential duration is abnormally long (e.g., prolonged QT).
Re-entry: Most commonly seen in structural heart diseases, with either functional re-entry circuits or anatomic circuits (e.g., scar/fibrosis).
- 2.
With this in mind, the most common primary precipitants of electrical storm can be thought of as those conditions that create or exacerbate one of these mechanisms [4].
Myocardial ischemia – frequently polymorphic VT/VF.
Drug toxicity.
Electrolyte abnormalities.
New/Decompensated heart failure – frequently monomorphic VT.
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