Winning teams have depth, and games are often won from the bench or deep in the batting order. That is certainly true when competing against ventricular fibrillation, and a few tools you might not know can help these patients.
A 55-year-old man with severe coronary heart disease and previous four-vessel coronary artery bypass surgery collapsed at a mall. He also had an unprotected left main atherosclerotic plaque. Bystanders immediately began chest compressions, and the available AED, unfortunately, advised no shock.
Paramedics started bag-valve-mask ventilation and high-quality mechanical compressions with a Lucas device. The initial rhythm was ventricular fibrillation, and multiple defibrillation attempts were unsuccessful. Amiodarone and epinephrine were given, along with more shocks between high-quality chest compressions without success.
The patient was intubated, and ventilations were provided with the ResQPod impedance threshold device. ACLS-driven resuscitation continued in the ED with defibrillation and additional doses of amiodarone, lidocaine, magnesium, epinephrine, and vasopressin, all with no return of spontaneous circulation. Cardiac ultrasound showed no organized cardiac activity.
Ventricular fibrillation is a rapidly fatal rhythm. Patients have no organized electrical activity or cardiac output. VF is often precipitated by myocardial ischemia, and it never terminates spontaneously. It is often the initiating event of sudden cardiac death. Treatments for ventricular fibrillation are directed at restoring perfusion to ischemic myocardium, correcting oxygenation and ventilation deficits, stabilizing the myocardium, and correcting electrolyte abnormalities.
The patient received high-quality uninterrupted CPR, electrical defibrillations, vasopressors, and antiarrhythmics, but still had persistent VF. Now what?
Patients who suffer a cardiac arrest and attempted resuscitation have elevated catecholamines, and they can be markedly elevated for those who have been treated with epinephrine (often multiple times). Epinephrine is a nonselective adrenergic agonist, stimulating β1, β2, and α receptors. The increased contractility, heart rate, automaticity, and peripheral vasoconstriction increase the work, oxygen consumption, and irritability of already damaged myocardial cells. The use of β-adrenergic receptor blockers to counter the effects of epinephrine and endogenous catecholamines is an option. Animal, retrospective, and small prospective studies support this. Early guidelines suggested propranolol after antiarrhythmics, but today esmolol is more effective. It provides short-acting β1-selective blockade, which allows it to exert its effect during the resuscitation with less long-term worsening of cardiogenic shock once spontaneous circulation is achieved.
Another option is high-energy defibrillation. Electricity works by depolarizing the myocardial cells and creating a zone of myocardium that has an extended refractory period. This zone stops the propagation of micro- and macro-reentrant activating circuits and wavelets. Atrial fibrillation and ventricular fibrillation are electrically stable rhythms, so larger proportions of the myocardium must be depolarized to terminate the rhythm.
Monophasic and biphasic are the most common waveform shapes used in external defibrillation. The polarity at each electrode in biphasic waveforms reverses part way through the defibrillation waveform. The use of a biphasic waveform in cardioversion and defibrillation increases defibrillation success by depolarizing more of the myocardium, and reduces the development of postshock arrhythmias. This is why biphasic waveforms have been universally adopted.
Similarly, using higher defibrillation voltages can also depolarize more of the myocardium. Original work on defibrillators did not find much more improvement in the defibrillation success rate above 200 J of biphasic energy, and patients had more postshock cardiogenic shock. But research now shows that using higher defibrillation voltages can be successful in refractory ventricular fibrillation when other treatments have failed. Described in animal models by Geddes in 1976 and Hoch in 1994, the use of up to 400 J on patients with refractory ventricular fibrillation during electrophysiology procedures restored regular rhythm.
Most defibrillators are limited to 200 J, so high-energy defibrillation is performed by attaching a second set of pads to a second defibrillator, allowing up to 400 J of biphasic energy to depolarize the myocardium. It is important to ensure that the vectors of both depolarization vectors pass through the heart. (See defibrillator pad placement for high-energy defibrillation in Figure 1 on p. 1.) Both shock buttons are pressed as simultaneously as possible. The high energy increases the likelihood of successful defibrillation, and the severity of post-resuscitation myocardial dysfunction increases with the magnitude of electrical energy delivered by the shock.
A third option that might seem way out there is a stellate ganglion blockade. The stellate ganglion is part of the sympathetic chain formed by the inferior cervical and first thoracic ganglia. It provides sympathetic innervation to the upper extremities, head, neck, and, most importantly for us, the heart. Blocking this nerve prevents sympathetic further cardiac stimulation. The procedure is usually performed under fluoroscopy for reflex sympathetic dystrophy, but it may be attempted by ultrasound guidance during resuscitation efforts for refractory ventricular fibrillation. The ganglion is located along the anterior spine, and is accessible by a percutaneous approach through the anterior neck. (Figures 2.) There is a risk, however, of residual left ventricular dysfunction. The blockade does not alter the circulating catecholamines, and is certainly a fourth-line treatment. Full details of this procedure can be found at http://bit.ly/1lvXSOK.
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