Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Do Emergency Physicians Intubate Often Enough to Maintain Competency?

 

    There is a study of the frequency of intubation among emergency physicians in the current Annals of Emergency Medicine. This study is accompanied by a discussion, which unfortunately does not question the assumption that intubation improves outcome. There is very little evidence to suggest that intubation improves outcomes. That evidence is only using paramedics with the highest success rates – much higher than your average paramedic.

 
Greater intubation experience in paramedics is associated with improved patient outcomes2; does a similar relationship exist for emergency physicians?[1]
 


Image credit.

The unquestioned assumption is that excellent intubation performance improves outcomes, rather than that excellent intubation performance causes less harm than average intubation performance, or below average performance. We do not have any good evidence to support the wishful thinking that paramedics, or even much more experienced emergency physicians, improve outcomes by intubating patients. We just assume this, because we don’t really want to know. If we decide to be honest and actually find out the effect of intubation, how will we handle it if the results show that we are harming more patients than we are helping?

The Cardiac Arrhythmia Suppression Trial was only started because the proponents of the different antiarrhythmics (encainide, flecainide, and moricizine) wanted to prove that their drug was better than all of the rest. They even agreed to include a placebo arm, although the doctors did not like the idea of depriving patients of such beneficial treatment.

 
CONCLUSIONS: There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide.[2]
 

People who had frequent ectopic heart beats – PVCs (Premature Ventricular Contractions) after a heart attack were more likely to die than people who did not have frequent PVCs. The obvious solution – the equivalent of intubation and blood-letting – was to give drugs that will get rid of the PVCs. The problem is that the PVCs were not the problem. The PVCs were just a sign of the problem. The drugs made the actual problem with the heart worse, while making the heart appear to be better. The same is true of blood-letting and may be true of intubation. Abundant evidence for the obvious benefits of blood-letting are quoted in the footnotes.[3]

If intubation is harmful, do we want to know?

If intubation by the average paramedic is harmful, do we want to know?

If intubation by the average emergency physician is harmful, do we want to know?

It isn’t as if we take intubation seriously. If we did take intubation seriously, we would practice much, much more than we do. In stead, we make excuses for failing to practice something that we claim is life-saving, because we are too arrogant to admit that practice is important to develop and maintain any skill.

Practicing on even the most basic mannequin should be done before every shift, whether you are a paramedic or an emergency physician. Unless you have a 99%, or better, success rate on hundreds of patients.

Footnotes:

[1] Intubation by Emergency Physicians: How Often Is Enough?
Kerrey BT, Wang H.
Ann Emerg Med. 2019 Dec;74(6):795-796. doi: 10.1016/j.annemergmed.2019.06.022. Epub 2019 Aug 19. No abstract available.
PMID: 31439364

The article above is commentary on the article below:

Procedural Experience With Intubation: Results From a National Emergency Medicine Group.
Carlson JN, Zocchi M, Marsh K, McCoy C, Pines JM, Christensen A, Kornas R, Venkat A.
Ann Emerg Med. 2019 Dec;74(6):786-794. doi: 10.1016/j.annemergmed.2019.04.025. Epub 2019 Jun 24.
PMID: 31248674

[2] Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al.
N Engl J Med. 1991 Mar 21;324(12):781-8.
PMID: 1900101

Free Full Text from N Engl J Med.

[3] Blood-Letting
Br Med J.
1871 March 18; 1(533): 283–291.
PMCID: PMC2260507
 

Physicians observed of old, and continued to observe for many centuries, the following facts concerning blood-letting.

1. It gave relief to pain. . . . .

2. It diminished swelling. . . . .

3. It diminished local redness or congestion. . . . .

4. For a short time after bleeding, either local or general, abnormal heat was sensibly diminished.

5. After bleeding, spasms ceased, . . . .

6. If the blood could be made to run, patients were roused up suddenly from the apparent death of coma. (This was puzzling to those who regarded spasm and paralysis as opposite states; but it showed the catholic applicability of the remedy.)

7. Natural (wrongly termed ” accidental”) hacmorrhages were observed sometimes to end disease. . . . .

8. . . . venesection would cause hamorrhages to cease.
 

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Does Room Air Reduce Mortality Among Term Neonates Requiring Respiratory Support at Birth?

     

The title of this meta-analysis suggests that it is important for us to have evidence in order to withhold treatments that are based on assumptions and anecdotes, rather than based on evidence. We should not even suggest this. Fortunately, the neonatal resuscitation guidelines have recommended not using the assumption-based and anecdote-based treatment since 2010.

 

Before 2000, resuscitation guidelines recommended 100% Fio2 for newborn respiratory support.6 However, hyperoxemia caused by high Fio2 results in the formation of free radicals, which can damage the lungs, brain, eyes, and other organs.7 Hypoxemia may also lead to harm. Literature in the early 2000s suggested no harm with room air resuscitation in term neonates, but also potentially an improvement in short-term mortality.8 In accordance with this literature, in 2010 and 2015 ILCOR recommended using room air for the initial resuscitation of term neonates.9, 10 [1]
 

The authors of this summary of the meta-analysis qualify this meta-analysis with a list of the weaknesses of the research. This is important for every analysis of research, but is it relevant, when there is no good reason to recommend the traditional intervention?  

According to these results with low evidence certainty, room air reduces short-term mortality compared with 100% Fio2 among term neonates requiring respiratory support at birth. Despite the low-quality evidence, these results are consistent across studies with low heterogeneity. The effect of intermediate Fio2 levels is not known and may benefit from further study. [1]
 

These are not reasons to reconsider, or oppose, the withholding of any treatments that are based on assumptions and anecdotes, rather than based on evidence.

The burden of proof is on those promoting any intervention. In the absence of valid evidence, we should limit ourselves to interventions that are supported by high quality evidence.

For epinephrine in cardiac arrest, there is no high quality evidence of benefit. The highest quality evidence is evidence of harm from epinephrine. The same is true for amiodarone, ventilation in cardiac arrest not due to a respiratory problem, furosemide in ADHF/CHF (Acute Decompensated Heart Failure/Congestive Heart Failure), and many other treatments we provide to patients, but definitely not for the benefit of patients.

We need to stop putting patients last in treatment decisions. The neonatal resuscitation guidelines are correct in their rejection of supplemental oxygen for neonatal resuscitation and the guidelines should not be changed.

Footnotes:

[1] Does Room Air Reduce Mortality Among Term Neonates Requiring Respiratory Support at Birth?

Brit Long, MD (EBEM Commentator), Michael D. April, MD, DPhil (EBEM Commentator) Department of Emergency Medicine, San Antonio Uniformed Services Health Education Consortium, Fort Sam Houston, TX

Annals of Emergency Medicine

October 2019, Volume 74, Issue 4, Pages 509–511

DOI:&nbps;https://doi.org/10.1016/j.annemergmed.2019.03.017

Free Full Text from Annals of Emergency Medicine. .

Happy Full Moon Friday the 13th


Technically, the full moon is not until 00:33 – 33 minutes after the end of Friday the 13th, so that may help the superstitious to feel better, since these superstition events are not actually coinciding – pitting twice as many Gods against the superstitious (a double whammy). Or the superstitious may feel worse, because they now have two days in a row of the Gods conspiring against them. The reality is that only their own beliefs conspire against them. it is all in the heads of the believers.

Even when someone does claim to come up with some evidence to support their beliefs, those conclusions are not supported by higher quality research.
 

In conclusion, Friday the 13th appears to be dangerous for some women. Since Friday falls on the 13th day of the month only twice a year on average, prospects for significant public health gains are limited. However, the risk of death for women who venture into traffic on this unlucky day is higher by 63%, and it should be possible to prevent one-third of the deaths occurring on this particular day. Even then, the absolute gain would remain marginal, since only one death per 5 million person-days could be prevented.[1]

 

The total number of deaths is small. Drawing that conclusion, based on a small sample size is a problem. In order to be able to come up with larger numbers, to minimize the effects of the small sample size, other researchers looked at the motor vehicle collisions, rather than just fatal motor vehicle collisions. The assumption that the cause of the fatalities was anxiety, produced by superstition among the drivers is projecting a lot onto the drivers – without any evidence to support this supposed cause.

It should not be a surprise that the results of a much larger sample size contradicts the assumptions based on the much smaller sample.
 

Conclusion:
We conclude that, in the Finnish traffic accident statistics for 1989–2002, females have not incurred more injury (or fatal) road traffic accidents on Fridays the 13th than expected, as a driver, bicyclist or pedestrian. We suggest that Näyhä’s contradicting result on fatalities is due to different sampling, non-optimal setting and chance in a fairly small data. However, this does not imply a nonexistent effect on accident risk as no exposure-to-risk data [18] are available. People who are anxious of “Black Friday” may stay home, or at least avoid driving a car. The only relevant data [4], suggesting a small decrease in highway traffic, is rather limited and should be confirmed with more extensive research.[2]

 

The law of small numbers is an attempt to expose the mistake of extrapolating from small numbers as if the small numbers are representative. Small numbers are misleading. Small numbers are often used to promote ideas that are not supported by adequate numbers – such as the claims that epinephrine improves cardiac arrest outcomes that matter, or that amiodarone improves cardiac arrest outcomes that matter.[3]

Footnotes:

[1] Traffic deaths and superstition on Friday the 13th.
Näyhä S.
Am J Psychiatry. 2002 Dec;159(12):2110-1.
PMID: 12450968

[2] Females do not have more injury road accidents on Friday the 13th.
Radun I, Summala H.
BMC Public Health. 2004 Nov 16;4:54.
PMID: 15546493

Free Full Text from PubMed Central.

[3] Chapter 10
The Law of Small Numbers

Thinking, Fast and Slow
Daniel Kahneman
2011
Wikipedia page

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Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction

 

Is prehospital use of NTG (NiTroGlycerin; GTN GlycerylTriNitrate in Commonwealth countries) safe for treating prehospital suspected STEMI (ST segment Elevation Myocardial Infarction) patients?

The evidence is limited, but does not suggest that prehospital NTG produces enough harm to discourage use in suspected STEMI. These researchers looked at the emergency department assessments of patients following prehospital NTG for suspected STEMI.  

Despite the theoretical risk, the limited retrospective studies of NTG in the prehospital setting for multiple indications suggest that the medication is safe.(10-13) However, with regard to NTG use for STEMI, the AHA International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care concluded that there was not enough evidence to determine the benefit or harm of out-of-hospital use of NTG.(14) Given the high false positive rates for STEMI identified in the field, an additional concern is that many patients treated with NTG for presumed STEMI will ultimately have an alternate etiology for their pain.(15, 16) Therefore, it is not clear that the benefits outweigh the risks of administering NTG to all patients with suspected STEMI in the field.[1]
 

This paper helps to show the safety of prehospital NTG for suspected STEMI, providing evidence that blood pressure changes were similar in suspected STEMI patients with an SBP (Systolic Blood Pressure) of 100, or higher, regardless of whether they were treated with NTG. The study is a retrospective chart review, so we do not know why some of the patients were not treated with NTG.

One reason mentioned, but not discussed, is that only 22% (96 of 440) suspected STEMI patients not treated with NTG are documented to have had pain, but there is no information on the type of pain or other cardiac symptoms of the patients. Were the paramedics avoiding treating atypical chest pain, such as pressure, heaviness, gastric discomfort, difficulty breathing, et cetera? We do not know. Was only chest pain being documented, rather than shoulder, or arm, or jaw, pain? We do not know. Did the pain resolve prior to EMS arrival? We do not know. Were the paramedics correctly recognizing when the machine interpretation of the ECGs (ElectroCardioGrams) were wrong? We do not know.

The median Initial Pain Score is documented as 8, with an IQR (Inter-Quartile Range) of 5-9 for those treated with NTG. For those not treated with NTG the Initial Pain Score is documented as 0, with an IQR of 0-0. We do not know the Initial Pain Score of those who did have pain, but were not treated with NTG. All of these patients were in an IQR that was not documented in the paper. The good news is that the suspected STEMI patients not treated with NTG act as a control group, although possibly with important differences that are not discussed in the paper.

Click on the image of the LA County protocol to make it larger.[2]

What about the 17% of suspected STEMI patients with SPB <100 mmHg who were treated with NTG?

Was medical command (California has certified MICNs [Mobile Intensive Care Nurses] providing medical command on the radio, with physicians available, as well) contacted for authorization to deviate from the protocol? If so, that is something that should be documented in the charts, which were reviewed for this paper. That information is not included in this paper. Those patients are much more interesting to me.

I do not object to using NTG to treat suspected STEMI with an SBP below 100 mmHg, but the authors seem to think that EMS should not even consider it. Do the outcomes of those patients support the approach of the authors? We do not know.

I suspect that the fears of bottoming out the blood pressure are very exaggerated, but it would be nice to have some evidence either way.

An important secondary end point was the differences between those with inferior/right ventricular STEMI, but treated with NTG.  

By vasodilating all blood vessels, and the venous system in particular, it causes a drop in blood pressure and preload. Thus, there is concern for precipitating hypotension in ACS involving the right ventricle.(1-3) Contraindications to the use of NTG, as outlined by the American Heart Association (AHA) Guidelines on the treatment of ACS, include right ventricular infarction.(4) This raises concern for use in inferior ST-segment elevation myocardial infarction (STEMI) in the prehospital setting, since many inferior STEMI result from proximal right coronary artery (RCA) occlusion and 50% involve the right ventricle.(3) Traditional 12-lead ECG is focused mainly on the left side of the heart and typically EMS protocols do not include acquisition of right-sided ECG leads. Further, in many systems, Basic Life Support (BLS) protocols allow for administration of NTG without differentiating the location of STEMI. There is also risk of other adverse events including bradycardia and cardiac arrest.(5-9)[1]
 

I have aggressively promoted the use of NTG for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). Many physicians are not comfortable with that, even though the available evidence shows that aggressive IV NTG doubled the survival rate for these hypotensive patients. More research is needed on the use of NTG, especially in hypotensive patients.  

Further, we did not find an increased risk of hypotension among patients with proximal or mid RCA occlusions confirmed on coronary angiography. There are several possible reasons for our findings. First, while right ventricular involvement in inferior STEMI is common, hemodynamic instability is actually rare due to the right ventricle’s more favorable oxygen supply-demand ratio compared to the left heart and more extensive collateral flow.(3, 22) In addition, left heart occlusions may also involve the right ventricle and result in a preload dependent condition.(23-25) While limited by sample size, our results suggests that specifically avoiding NTG use in inferior STEMI, which is common in EMS systems, may be misguided. One quarter of the local EMS agencies in the state of California, for example, currently prohibit the use of NTG in inferior STEMI.(26) This analysis would benefit from additional study with a larger sample size and specific information about the infarct territory. Further studies are needed to determine which patients, in particular, are at increased risk for hypotension when treated with NTG.[1]
 

Perhaps NTG is also safe for treating patients with inferior ischemia and even right ventricular ischemia.

Footnotes:

[1] Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction.

Bosson N, Isakson B, Morgan JA, Kaji AH, Uner A, Hurley K, Henry TD, Niemann JT.

Prehosp Emerg Care. 2018 Dec 17:1-9. doi: 10.1080/10903127.2018.1558318. [Epub ahead of print]

PMID: 30556765

[2] Treatment Protocol: Chest Pain */ Acute MI

Reference No. 1244

LA County Paramedic Protocols

Los Angeles County Department of Health Services – Emergency Medical Services

Protocol

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Association of ventilation with outcomes from out-of-hospital cardiac arrest

 

Does this study compare chest compressions with pauses for ventilation (regular CPR [CardioPulmonary Resuscitation]) against continuous chest compressions with no ventilations (compression-only CPR)?

Absolutely not.

This only compares compressions with pauses for good ventialtions against compressions with pauses for bad ventilations.

Will this be used to justify including ventilations in CPR, in spite of the absence of any valid evidence that ventilations improve outcomes?

Yes. It already has in the editorial about the study, published in the same issue.[1]

The authors of the paper were clear about the actual comparison in the discussion.
 

Why did so few patients in our study receive ventilation during CPR? Ventilation with a BVM device is a difficult skill to perform properly and must be practiced to maintain proficiency.22 The person performing ventilation must extend the neck, or place an oral airway, and/or perform a jaw thrust maneuver in order to maintain an open airway, a tight mask seal on the face must be maintained to prevent air from leaking around the mask, and the rescuer must then simultaneously squeeze the manual ventilator over 1 to 1.5 s. Our study showed no significant difference in the number of pauses between Group 1 and Group 2 patients (11 vs. 12 pauses). However, Group 2 patients received significantly more ventilations than Group 1 patients (8 vs. 3 ventilations). The study suggests that the rescuers in both Groups attempted ventilation about the same number of times per patient, but these attempts frequently did not result in lung inflation in Group 1 patients.[2]

 

In other words, this is a study of 30 compressions with a pause for 2 adequate ventilations to 30 compressions with a pause for 2 inadequate ventilations. This is important to know, but it has nothing to do with compression-only resuscitation.
 


 

Were the ventilations in the bad ventilation group going into the stomach? There are not a lot of possibilities, but not much of the ventilations were not going into the lungs or the ventilations were very shallow.

The authors do not mention if there is any difference in the rate of vomiting, aspiration, or other side effects expected from bad ventilation, between the groups.

The authors appear to be measuring the quality of ventilation, which is has never been shown to improve outcomes over compression-only resuscitation.

There is research showing that ventilations do not improve outcomes:
 

Cardiocerebral resuscitation improves survival of patients with out-of-hospital cardiac arrest.
Kellum MJ, Kennedy KW, Ewy GA.
Am J Med. 2006 Apr;119(4):335-40.
PMID: 16564776 [PubMed – indexed for MEDLINE]

Cardiocerebral resuscitation improves neurologically intact survival of patients with out-of-hospital cardiac arrest.
Kellum MJ, Kennedy KW, Barney R, Keilhauer FA, Bellino M, Zuercher M, Ewy GA.
Ann Emerg Med. 2008 Sep;52(3):244-52. Epub 2008 Mar 28.
PMID: 18374452 [PubMed – indexed for MEDLINE]

Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest.
Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA, Richman PB, Kern KB.
JAMA. 2008 Mar 12;299(10):1158-65.
PMID: 18334691 [PubMed – indexed for MEDLINE]

Free Full Text at JAMA

Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest.
Bobrow BJ, Ewy GA, Clark L, Chikani V, Berg RA, Sanders AB, Vadeboncoeur TF, Hilwig RW, Kern KB.
Ann Emerg Med. 2009 Nov;54(5):656-662.e1. Epub 2009 Aug 6.
PMID: 19660833 [PubMed – indexed for MEDLINE]

And more.

 

 

Footnotes:

[1] Ventilation during cardiopulmonary resuscitation-Only mostly dead!
Mosesso VN Jr.
Resuscitation. 2019 Aug;141:200-201. doi: 10.1016/j.resuscitation.2019.06.274. Epub 2019 Jun 22. No abstract available.
PMID: 31238035

 

[2] Association of ventilation with outcomes from out-of-hospital cardiac arrest.
Chang MP, Lu Y, Leroux B, Aramendi Ecenarro E, Owens P, Wang HE, Idris AH.
Resuscitation. 2019 Aug;141:174-181. doi: 10.1016/j.resuscitation.2019.05.006. Epub 2019 May 18.
PMID: 31112744

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How Effective Is Epinephrine for Improving Survival Among Patients in Cardiac Arrest?

   

There have been two studies comparing epinephrine with placebo to treat out of hospital cardiac arrest. The Jacobs study was stopped early, because of interference by those who do not want to know if their medicine actually works.[1] The purpose of research is to determine, as objectively as possible, if a treatment is better than placebo nothing.  

Click on the image to make it larger.  

Even the small sample size shows a impressive p values of <0.001 for both ROSC (Return Of Spontaneous Circulation) and being admitted to the hospital. Unfortunately, that does not lead to outcomes that are better than placebo.

The Perkins study (PARAMEDIC2) did not find a significant difference between adrenaline (epinephrine in non-Commonwealth countries) and placebo.[2] The Jacobs study also did not find a difference, but the numbers were small, due to the interference by the less than knowledgeable. Following the Jacobs study, some intervention proponents have suggested that the problem is not a lack of evidence of benefit, but need to look at the evidence from the right perspective. The inadequate evidence is not “inadequate”, but really just misunderstood. All we need to do is use a method of analysis that compensates for the tiny sample size. A Bayesian approach will produce the positive outcome that is not justified by so few patients.[3]

What happens when the numbers are combined, so that the sample size is large enough to eliminate the need for statistical chicanery to come up with something positive?

The outcomes do not improve.  

Neither standard dose adrenaline, high-dose adrenaline,vasopressin nor a combination of adrenaline and vasopressin improved survival with a favourable neurological outcome.[4]
 

If the Bayesian approach were appropriate, then the much larger sample size would have provided more than enough patients to confirm the optimism of the epinephrine advocates. The result is still not statistically significant. Maybe a much, much larger study will show a statistically significant, but tiny, improvement in outcomes with epinephrine, but don’t hold your breath for that. It took half a century to produce the first study, then seven more years for the second. With the cost of research and the problems coordinating such a large study, it is more likely that the guidelines will continue to recommend spending a lot of time and money giving a drug that diverts attention from the interventions that do improve outcomes.

There is still no evidence that adrenaline provides better outcomes than placebo in human cardiac arrest patients.

  –  

Footnotes:

  –  

[1] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Resuscitation. 2011 Sep;82(9):1138-43. doi: 10.1016/j.resuscitation.2011.06.029. Epub 2011 Jul 2. PMID: 21745533

Free Full Text PDF Download from semanticscholar.org  

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

  –  

[2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators. N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18. PMID: 30021076

Free Full Text from N Engl J Med.

  –  

[3] Regarding “Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial”. Youngquist ST, Niemann JT. Resuscitation. 2012 Apr;83(4):e105; author reply e107. doi: 10.1016/j.resuscitation.2011.09.035. Epub 2012 Jan 18. No abstract available. PMID: 22266068

Free Full Text from Resuscitation.

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[4] Adrenaline and vasopressin for cardiac arrest. Finn J, Jacobs I, Williams TA, Gates S, Perkins GD. Cochrane Database Syst Rev. 2019 Jan 17;1:CD003179. doi: 10.1002/14651858.CD003179.pub2. PMID: 30653257    

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Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest

   

This is an animal study, rather than a human study, but it has fewer disadvantages than the usual animal studies of medical cardiac arrest. Animals do not develop the comorbidities that humans do, but have artificially created heart attacks, rather than by the development of actual heart disease. In studying trauma, this is less of a problem, since trauma is artificially created. This study is much more representative of penetrating injuries with a low velocity objects, than blunt force trauma, or penetrating injury with a high velocity object.

Are we really killing trauma patients with our chest compressions?

Maybe. This is one small study (39 pigs), but it does raise questions about the ways we can minimize the harm we cause.

 

 
CCC were associated with increased mortality and compromised haemodynamics compared to intravenous fluid resuscitation. Whole blood resuscitation was better than saline.[1]

 
A soft tissue injury was created, with 3 shots to the right thigh using a captive bolt (Cash Special, Accles and Shelvoke, Sutton Coldfield, UK). Two minutes later animals underwent a controlled haemorrhage (30% blood volume) at an exponentially reducing rate as previously described12 until the mean arterial blood pressure (MAP) was 45 mmHg. Blood was collected into CPD (citrate phosphate dextrose) and stored at room temperature until required for later transfusion.[1]
 

Image source

 

This study, conducted in an animal model of haemorrhage-induced traumatic cardiac arrest, has demonstrated that chest compressions confer no benefit over fluid resuscitation alone, and blood should be the fluid therapy of choice.[1]

  That seems to be concluding too much, since this is just one study, but it does reinforce the results of other, similar studies. We should study the outcomes in humans, since there does appear to be equipoise. There never was a physiological justification for chest compressions in traumatic cardiac arrest which appears to be due to hemorrhage. Now there is more evidence that chest compressions produce more harm than benefit in traumatic cardiac arrest which appears to be due to hemorrhage.

 
One study using a baboon traumatic cardiac arrest model found that the improvements in haemodynamics seen with chest compressions for normovolaemic cardiac arrest were not reproduced in hypovolaemic arrest.14 The authors suggested that CCC should not delay correction of the underlying deficit causing TCA, but the study was undertaken in only three animals, perhaps limiting its clinical relevance. A more recent study using a canine model of pulseless electrical activity in TCA found no benefit of chest compressions over fluid therapy alone or fluid combined with chest compressions; in fact the chest compression only group had worse survival, base deficit and ejection fraction.15 The authors concluded that further research was required to determine whether CPR has a role for the patient in haemorrhagic shock.[1]

  Most important is that the outcome is ROSC (Return Of Spontaneous Circulation), not return to normal neurological function. Since these are pigs, even the appearance of normal neurological function may not mean anything in humans. Still, the treatment is not evidence-based, so there does not appear to be a good reason to prefer to continue using compressions for traumatic cardiac arrest which appears to be due to hemorrhage.

Here in America, we are unlikely to do the research, because we are more concerned with appearances than with improving outcomes for patients. Maybe somebody in Britain or Australia will have to demonstrate some responsibility, so we can stop using chest compressions to kill trauma patients.

  Footnotes:

  [1] Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest. Watts S, Smith JE, Gwyther R, Kirkman E. Resuscitation. 2019 May 9;140:37-42. doi: 10.1016/j.resuscitation.2019.04.048. [Epub ahead of print]

PMID: 31077754

Free Full Text from Resuscitation

  .

The Big Government, Big Religion, Immoral Opposition to Physician Assisted Suicide

 
 

The government should not force people to die painful deaths, in order to please the people who can only think of the ways something can go wrong and/or the Bible thumpers. These patients are not harming anyone else and we should stop condemning them as if they are the ones rejecting morality.

There are ways to protect vulnerable patients from being taken advantage of by family, or by others, without forcing everyone to die painfully. Physician assisted suicide is a way to protect vulnerable patients from being taken advantage of by those who claim to know what is best for everyone and want to force it on everyone, for their own good.

The alternative to physician assisted suicide is to require moral physicians break the law in order to provide the care the patient needs – relief of suffering that cannot otherwise be relieved. Physician assisted suicide should not be opposed by any ethical medical organization.

The older I get, the more I see patients abused by this hypocritical legal prohibition on ethical behavior.

Providing the care that the patient requests, with fully informed consent by the patient, is far more ethical than claiming that other people should control patients’ lives for the patients.

This does not affect me much, as a patient, because I can acquire whatever I need to end my life, whenever I feel it is the best option. I also have the ability to administer whatever medications I might choose to use, but I would probably have to do this sooner than I would like, in order to avoid having to rely on others to do what is right.

I will not ask anyone else to put themselves at legal risk, in order to allow me more time.

I will do whatever I need to do before I lose the ability to do everything on my own. Obviously, this will not apply to many medical conditions that have catastrophic sudden onset. I am not currently experiencing any symptoms and I do not have any diagnosis of any condition that would encourage me to end my life, but I may need to move to a state that does not require patients to be tortured to death, if that changes. If the SCOTUS literalists/originalists imposes a big government sharia decision to prohibit ethical end of life decisions by patients, then I might need to move to another country in order to have a longer life.

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