The impedance threshold device (ITD) is another new adjunct in cardiac arrest. This devicetemporarily prevents airflow through the bag-valve mask or endotracheal tube during chest expansion (decompression phase of CPR), thereby augmenting negative intrathoracic pressure and increasing venous return and cardiac output. The ResQTrial, which compared standard CPR to a combination of active compression-decompression CPRcoupled with an ITD improved survival in cardiac arrest from 6% to 9%.(4) Another trial using the ITD in pre-hospital cardiac arrest failed to show a benefit, but conclusions drawn from these data are limited because time to ITD placement was delayed.(5) There is some data from this trial which was discussed and which further supports ITD use, but which cannot be published here, as it will be published in July 2013 and is embargoed at the moment. The ITD should be used in conjunction with active compression-decompression CPR to fully realize the benefits of increased chest expansion with augmented negative intrathoracic pressure.
Hyperventilation is deadly: during cardiac arrest, it creates excessive positive intrathoracic pressure and decreases venous return and cardiac output. In an animal model, hyperventilation was associated with a decrease in coronary perfusion pressure and survival.(6) Patients in cardiac arrest should be ventilated at a rate of 10 breaths per minute.
Epinephrine, although featured in the ACLS cardiac arrest algorithm and used every day throughout the world, has never been shown to improve survival to hospital discharge. The benefits of epinephrine are currently limited only to increased rates of return of spontaneous circulation. Epinephrine is potentially harmful; in a recent large well-performed Japanese study pre-hospital epinephrine administration in cardiac arrest was associated with decreased survival and functional outcome at 1 month.(7) The best dose and time interval for epinephrine administration has not been defined, but because of these recent data it is prudent to minimize total epinephrine administered in cardiac arrest. Novel investigations into therapies such as nitroprusside that optimize blood flow instead of blood pressure are extremely promising, but have only been demonstrated in animal models.(8) (There are many more novel therapies being actively studied in the MMRF laboratory, especially by Drs. Yannopoulos and Lurie). Our patient received 8 mg of epinephrine and survived. How much did epinephrine contribute to his successful resuscitation, if at all?
In cases of refractory ventricular fibrillation or tachycardia, beta-blockade can result in less electrical instability. One might worry that it would contribute to cardiogenic shock, but, paradoxically, it has the potential to improve inotropy by relaxing the semi-permanent state of left ventricular (LV) contraction and functional mitral stenosis induced by epinephrine. It can thus improve LV filling and outflow. There are several case reports, as in this case, in which esmolol and other beta-blockers rapidly terminated refractory ventricular fibrillation and were associated with ROSC.(9,10) Certainly, administration of a beta-blocker should be strongly considered before terminating resuscitative efforts for a patient in incessant ventricular dysrhythmia.
Additionally, there are a number of case reports in which even beta-blockade was ineffective, but in which a bedside left stellate ganglion block was performed and immediately terminated ventricular fibrillation.(11-13) A recent post detailing this procedure can be found here: http://resusreview.com/2013/ultrasound-guided-stellate-ganglion-block-for-refractory-ventricular-fibrillation/
To the cath lab with ongoing chest compressions? Finally, patients who arrest while in the ED and cannot be resuscitated may survive if transported with ongoing mechanical CPR to the cardiac catheterization lab for restoration of flow to an occluded coronary artery. During the panel discussion, the question arose as to whether percutaneous coronary intervention (PCI) is more easily completed without the motion artifact of chest compressions, and the utility of initiating extracorporeal membrane oxygenation (ECMO) to create ideal procedural conditions (14). Dr. Yannopoulos, an interventional cardiologist and leading resuscitation researcher, stated that taking the time to place ECMO was not beneficial as PCI can readily be performed during chest compressions. ECMO can be placed in the cardiac catheterization lab or in the ICU after the procedure, if indicated. PCI during mechanical CPR is probably only warranted when the time between arrest and intervention is extremely short.
Finally, all patients who are comatose due to cardiac arrest should undergo therapeutic hypothermia (this is so well established that it needs no elaboration).
Key Points:• High-quality CPR is critical. Compressions should be 2” deep at a rate of 100 with fullchest recoil after each compression.• Mechanical CPR can provide high-quality, long-lasting CPR.• Active compression-decompression CPR with an ITD significantly increased survival incardiac arrest. These two adjuncts should always be used together to maximize benefit.• Hyperventilation is fatal. Bag at a rate of 10 ventilations per minute.• Epinephrine has no documented benefit of any clinical significance apart from ROSC,and may be harmful. Total epinephrine dosing in cardiac arrest should be limited.• Esmolol or other beta-blockers should be administered in refractory ventricularfibrillation, and can lead to rapid ROSC. Ultrasound-guided left stellate ganglion blocksare a last-line option for ventricular dysrhythmias that persist after all other therapies.
Use therapeutic hypothermia!
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