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Wow! Did anyone else hear the mental doors slamming shut? :shock:

The study that I referenced was begun in 2000, shortly after the last guideline revision. Dr. Ewy published his findings in 2003, and even presented them at the science gathering for the AHA before the latest guidelines came out. American Heart did not buy into them, because of the huge jump in the change from previous.

The ventilation numbers are staggering. You guys are absolutely correct. Now, if we think about what happens, they can be viewed as reasonable. The 37 ventilations/minute comes from a study that was done in several locations. The only one that I can remember is Milwaukee, but I know there were other places involved. Even after retraining, providers were only slowed down to the mid-20's for rate. No, they were not using a ventilator, only a BVM.

My view on this information is, if doing things a little differently will successfully resuscitate 2-3 more out of the 100 that I have to work on, then why not try it. If we are going to abuse a corpse, why not try something else. As the article states, if results improve only 10%, then wouldn't it be worth doing. Comparing to current/previous "guidelines", what would the harm be?

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I still question the science behind his conclusions, there are several studies that show it is not necessarily the ventilation's that are the problem but the high flow 02. Here is an abstract of one of those studies..

Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome.

Liu Y, Rosenthal RE, Haywood Y, Miljkovic-Lolic M, Vanderhoek JY, Fiskum G.

Department of Biochemistry and Molecular Biology, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA.

BACKGROUND AND PURPOSE: Increasing evidence that oxidative stress contributes to delayed neuronal death after global cerebral ischemia has led to reconsideration of the prolonged use of 100% ventilatory O2 following resuscitation from cardiac arrest. This study determined the temporal course of oxidation of brain fatty acyl groups in a clinically relevant canine model of cardiac arrest and resuscitation and tested the hypothesis that postischemic ventilation with 21% inspired O2, rather than 100% O2, results in reduced levels of oxidized brain lipids and decreased neurological impairment. METHODS: Neurological deficit scoring and high performance liquid chromatography measurement of fatty acyl lipid oxidation were used in an established canine model using 10 minutes of cardiac arrest followed by resuscitation with different ventilatory oxygenation protocols and restoration of spontaneous circulation for 30 minutes to 24 hours. RESULTS: Significant increases in frontal cortex lipid oxidation occurred after 10 minutes of cardiac arrest alone with no reperfusion and after reperfusion for 30 minutes, 2 hours, and 24 hours (relative total 235-nm absorbing peak areas=7.1+/-0.7 SE, 17.3+/-2.7, 14.2+/-3.2, 16.1+/-1.0, and 14.0+/-0.8, respectively; n=4, P<0.05). The predominant oxidized lipids were identified by gas chromatography/mass spectrometry as 13- and 9-hydroxyoctadecadienoic acids (13- and 9-HODE). Animals ventilated on 21% to 30% O2 versus 100% O2 for the first hour after resuscitation exhibited significantly lower levels of total and specific oxidized lipids in the frontal cortex (1.7+/-0.1 versus 3.12+/-0.78 microg 13-HODE/g wet wt cortex., n=4 to 6, P<0.05) and lower neurological deficit scores (45.1+/-3.6 versus 58.3+/-3.8, n=9, P<0.05). CONCLUSIONS: With a clinically relevant canine model of 10 minutes of cardiac arrest, resuscitation with 21% versus 100% inspired O2 resulted in lower levels of oxidized brain lipids and improved neurological outcome measured after 24 hours of reperfusion. This study casts further doubt on the appropriateness of present guidelines that recommend the indiscriminate use of 100% ventilatory O2 for undefined periods during and after resuscitation from cardiac arrest.

PMID: 9707212 [PubMed - indexed for MEDLINE]

I stand behind my statements, 37 is a damn high ventilation rate, in my experience I do not see someone ventilating at a rate that high for long. Also as I stated intubation secures the airway and an NRB, NPA or OPA does not. Dr Ewy also states that it will be a hard sell to stop Paramedics from intubating. That statement is false, it would be easy to get Para's to stop intubating, convince their Medical Director that intubation is unnecessary and they will not have a choice. Now that is going to be a hard sell.

Peace,

Marty

:thumbleft:

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That is part of the problem with medicine and especially EMS. Most do not know how to read a study and take at face value. It is a shame that statistics and Foundations of Research is not required in Paramedic school, so studies can be dissected and be really evaluated.

Look at the mean number and the population (P) and the standard deviation etc.... The same being of :

What type of patient criteria was used... down time.. previous cardiac hx., CPR how long ?.. etc..

What would be outcome would be without changes ?

Who sponsored this research ?

How active was the author in this research or where they more an editor ?

Again, if this works ..great ! But, please no not accept any changes solely based upon a few research articles. Even that this was performed in multiple sites does not impress me... so was Bretylium, high dose Epi, and even the Amway suction unit..

Time will tell.. again, research physicians should be held accountable... they are not! If the course that they predicted does not come true, they should be held accountable. Whenever; we start having some re-courses and responsibility associated with "too good to be true" statements, then we will start having credible research publicaitons.

R/r 911

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(Are the new resuscitation guidelines optimal?.

Cardiopulmonary resuscitation

Current Opinion in Critical Care. 12(3):193-197 @ June 2006.

Chamberlain, Douglas )

Abstract:

Purpose of review: The purpose of this review is to evaluate the 2005 guidelines on cardiopulmonary resuscitation.

Recent findings: International guidelines are based ideally on results from robust clinical trials. They are necessarily constrained in how far they can draw conclusions from experimental data, and have to pay regard to perceived safety and educational issues. Informed opinion can be more radical in drawing from compelling recent experimental findings, particularly when supported by unreplicated or indirect clinical evidence. Those already available cover a range of issues relevant to the guidelines; the most important ones are reviewed here.

Summary: The 2005 guidelines represent a major advance on those previously in use, but on the evidence already available they cannot be considered optimal. Deviations based on good evidence should not be discouraged provided they are approved and preferably monitored by authoritative bodies that should see this as a legitimate role in developing the science of resuscitation medicine. Guidelines for the most pressing of medical emergencies should not be set and inflexible over several years whilst the science behind them continues to advance.

(Haemodynamics of cardiac arrest and resuscitation.

Cardiopulmonary resuscitation

Current Opinion in Critical Care. 12(3):198-203 @ June 2006.

Andreka, Peter a; Frenneaux, Michael P B)

Abstract:

Purpose of review: This review will summarize the available data regarding the haemodynamic changes occurring following cardiac arrest in humans and animal models.

Recent findings: Following cardiac arrest due to ventricular fibrillation without cardiopulmonary resuscitation, blood flow exponentially falls but continues for approximately 5 min until the pressure gradient between the aorta and the right heart is completely dissipated. During cardiopulmonary resuscitation forward flow occurs into the aorta during the compression phase. Coronary blood flow is retrograde during the compression phase and antegrade during the decompression phase. Carotid blood flow takes over a minute to reach plateau levels following the initiation of chest compressions, and even brief interruptions of compressions result in a dramatic reduction in carotid blood flow which takes a minute or so to recover to plateau levels when compressions are reinstituted. Coronary perfusion pressure during the release phase of cardiopulmonary resuscitation has been shown to be a powerful predictor of the likelihood of recovery of spontaneous circulation following restoration of electrical activity.

Summary: Recent studies have provided important insights into the haemodynamics of cardiac arrest and of cardiopulmonary resuscitation which may inform more effective strategies for the management of cardiac arrest in the future.

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