Driver BE, Debaty G, Plummer DW, Smith SW. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation. 2014 PMID: 25033747
A case series describing the successful use of an esmolol bolus and then infusion for treatment of refractory VFib in 6 patients. Great description and something to consider when next faced with the patient who, despite multiple shocks and other meds, does not return to spontaneous circulation.
Recommended by: Jeremy Fried
Read more: 68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest. (Dr. Smith’s ECG Blog)
Local Anesthetic Toxicity - Don’t Follow ACLS
Systemic toxicity of local anesthetics can occur after administration of an excessive dose or because of accidental intravascular injection. If malignant arrhythmias occur, ACLS must be modified. Epinephrine can induce dysrhythmias or it can exacerbate the ongoing arrhythmia associated with local anesthetic overdose. Consequently, vasopressin use may be more appropriate to maintain the BP, support coronary perfusion, and facilitate local anesthetic metabolism (2). In addition, avoid treating arrhythmias with lidocaine since treating local anesthetic-induced arrhythmias with another local anesthetic is likely to add to the cardiotoxicity.
(2) Krismer AC, et al. Anesth Analg Â 2001;93(3):734-42.
eradstveit BE, Heltne JK. PQRST – A unique aide-memoire for capnography interpretation during cardiac arrest. Resuscitation 2014 PMID 25063372
End tidal CO2 monitoring has become a mainstay in resuscitation. This article gives a mnemonic device for applying capnography during resuscitation. This tool can help bridge the gap from theory to application for many practitioners.
P – Position of the tube
Q – Quality of compressions
R – Return of spontaneous circulation
S – Strategy for further treatment
T – Termination of resuscitation
Today on the podcast, I address the last little bit from my SMACC lecture on the new management of the intra-arrest: hemodynamic, individualized dosing of epinephrine.
The podcast is interspersed with clips from Professor Norman Paradis
Articles/Posts on Epinephrine by ACLS Guidelines
(Stiell et al. 2004)*,
(Donnino et al. 2014)*
(Olasveengen et al. 2009)*
Epinephrine Dosing Based on DBP
Three Swine Study
(Crit Care Med. 2013 Dec;41(12):2698-704)
(Resuscitation. 2013 May;84(5):696-701)
(Friess et al. 2014)*
Here is the abstract from the latter study:
AIM: Advances in cardiopulmonary resuscitation (CPR) have focused on the generation and maintenance of adequate myocardial blood flow to optimize the return of spontaneous circulation and survival. Much of the morbidity associated with cardiac arrest survivors can be attributed to global brain hypoxic ischemic injury. The objective of this study was to compare cerebral physiological variables using a hemodynamic directed resuscitation strategy versus an absolute depth-guided approach in a porcine model of ventricular fibrillation (VF) cardiac arrest.
METHODS: Intracranial pressure and brain tissue oxygen tension probes were placed in the frontal cortex prior to induction of VF in 21 female 3month old swine. After 7minutes of VF, animalswere randomized to receive one of three resuscitation strategies: 1) Hemodynamic Directed Care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100mmHg and titration of vasopressors to maintain coronary perfusion pressure (CPP)> 20mmHg; 2) Depth 33mm(D33): target CC depth of 33mm with standard American Heart Association (AHA) epinephrine dosing; or 3) Depth 51mm(D51): target CC depth of 51mm with standard AHA epinephrine dosing.
RESULTS: Cerebral perfusion pressures (CerePP )were significantly higher in the CPP-20 group compared to both D33 (p<0.01) and D51 (P=0.046), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Brain tissue oxygen tension was also higher in the CPP-20 group compared to both D33 (P<0.01) and D51 (P=0.013), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Subjects with a CPP>20mm Hg were 2.7 times more likely to have a CerePP>30mm Hg (P< 0.001).
CONCLUSIONS: Hemodynamic directed resuscitation strategy targeting coronary perfusion pressure>20mmHg following VF arrest was associated with higher cerebral perfusion pressures and brain tissue oxygen tensions during CPR. University of Pennsylvania IACUC protocol #803026.
Human Study by Dr. Paradis
Coronary Perfusion Pressure and the Return of Spontaneous Circulation in Human Cardiopulmonary Resuscitation
Coronary perfusion pressure (CPP), the aortic-to-right atrial pressure gradient during the relaxation phase of cardiopulmonary resuscitation, was measured in 100 patients with cardiac arrest. Coronary perfusion pressure and other variables were compared in patients with and without return of spontaneous circulation (ROSC). Twenty-four patients had ROSC. Initial CPP (mean±SD) was 1.6 ± 8.5 mm Hg in patients without ROSC and 13.4 ± 8.5 mm Hg in those with ROSC. The maximal CPP measured was 8.4 ±10.0 mm Hg in those without ROSC and 25.6 ±7.7 mm Hg in those with ROSC. Differences were also found for the maximal aortic relaxation pressure, the compression-phase aortic-to— right atrial gradient, and the arterial Po2. No patient with an initial CPP less than 0 mm Hg had ROSC. Only patients with maximal CPPs of 15 mm Hg or more had ROSC, and the fraction of patients with ROSC increased as the maximal CPP increased. A CPP above 15 mm Hg did not guarantee ROSC, however, as 18 patients whose CPPs were 15 mm Hg or greater did not resuscitate. Of variables measured, maximal CPP was most predictive of ROSC, and all CPP measurements were more predictive than was aortic pressure alone. The study substantiates animal data that indicate the importance of CPP during cardiopulmonary resuscitation.
Good Review on Epinephrine
AHA Cardiopulmonary Resuscitation Quality Statement
by Meaney P. et al (Circulation 2013;128:417)
<12 BPM, Minimal Chest Rise
Just Art Line DBP>25-30 (I disagree)
ETCO2>20 mm Hg
If DBP < 20 optimize compressions or vasopressors (Circulation 2011;123:e236)
CVP can be higher during the poor flow of the arrest state (Sanders, Ogle, and Ewy 1985)*,(Am J Emerg Med. 1985 Jan;3(1):11-4.), and (Martin et al. 1986)* and this one had a mean of 16 (N. A. Paradis et al. 1989)*
so I would shoot for 35-40 mm Hg
Goal is to give less epineprhine
Hemodynamic-directed CPR Review
(Sutton et al. 2014)*
Now on to the Podcast…
Podcast: Play in new window | Download (16.9MB)
Donnino, Michael W, Justin D Salciccioli, Michael D Howell, Michael N Cocchi, Brandon Giberson, Katherine Berg, Shiva Gautam, and Clifton Callaway. 2014. Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry. BMJ (Clinical research ed.) (May 20). doi:10.1136/bmj.g3028. http://www.ncbi.nlm.nih.gov/pubmed/24846323.
Friess, Stuart H, Robert M Sutton, Benjamin French, Utpal Bhalala, Matthew R Maltese, Maryam Y Naim, George Bratinov, et al. 2014. Hemodynamic directed CPR improves cerebral perfusion pressure and brain tissue oxygenation. Resuscitation (June 16). doi:S0300-9572(14)00589-9. http://www.ncbi.nlm.nih.gov/pubmed/24945902.
Martin, G B, D L Carden, R M Nowak, J R Lewinter, W Johnston, and M C Tomlanovich. 1986. Aortic and right atrial pressures during standard and simultaneous compression and ventilation CPR in human beings. Annals of emergency medicine, no. 2. http://www.ncbi.nlm.nih.gov/pubmed/3946853.
Olasveengen, Theresa M, Kjetil Sunde, Cathrine Brunborg, Jon Thowsen, Petter A Steen, and Lars Wik. 2009. Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA : the journal of the American Medical Association, no. 20 ( 25). doi:10.1001/jama.2009.1729. http://www.ncbi.nlm.nih.gov/pubmed/19934423.
Paradis, N. A., G. B. Martin, M. G. Goetting, J. M. Rosenberg, E. P. Rivers, T. J. Appleton, and R. M. Nowak. 1989. Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms. Circulation. Ovid Technologies (Wolters Kluwer Health), August 1. http://dx.doi.org/10.1161/01.CIR.80.2.361.
Paradis, Norman A. 1990. Coronary Perfusion Pressure and the Return of Spontaneous Circulation in Human Cardiopulmonary Resuscitation. JAMA: The Journal of the American Medical Association. American Medical Association (AMA), February 23. http://dx.doi.org/10.1001/jama.1990.03440080084029.
Sanders, A B, M Ogle, and G A Ewy. 1985. Coronary perfusion pressure during cardiopulmonary resuscitation. The American journal of emergency medicine, no. 1. http://www.ncbi.nlm.nih.gov/pubmed/3970745.
Stiell, Ian G, George A Wells, Brian Field, Daniel W Spaite, Lisa P Nesbitt, Valerie J De Maio, Graham Nichol, et al. 2004. Advanced cardiac life support in out-of-hospital cardiac arrest. The New England journal of medicine, no. 7 ( 12). http://www.ncbi.nlm.nih.gov/pubmed/15306666.
Sutton, Robert M, Stuart H Friess, Matthew R Maltese, Maryam Y Naim, George Bratinov, Theodore R Weiland, Mia Garuccio, et al. 2014. Hemodynamic-directed cardiopulmonary resuscitation during in-hospital cardiac arrest. Resuscitation, no. 8 (April 28). doi:10.1016/j.resuscitation.2014.04.015. http://www.ncbi.nlm.nih.gov/pubmed/24783998.