I have put together a capnography tutorial for your education and enjoyment. The videos below are the capnography tutorial. There are 7 lessons, consisting of relatively short videos.
Adam Thompson, EMT-P
I have put together a capnography tutorial for your education and enjoyment. The videos below are the capnography tutorial. There are 7 lessons, consisting of relatively short videos.
Adam Thompson, EMT-P
There are many things that will lengthen the QT segment, but how much should we worry when the patient has a long QT segment, or when giving the patient a treatment that lengthens the QT segment? Are there some things that, even though they may lengthen the QT segment, may protect the heart from arrhythmia at the same time?
This prospective study was conducted to evaluate the frequency of malignant arrhythmias and to analyse the possible effect of hypothermia on the QTc interval using a continuous Holter ECG during MTH treatment.
Mild therapeutic hypothermia (MTH in the paper) is one of condition these authors wanted to investigate to find out if it really does cause QT prolongation and if that QT prolongation might be dangerous. Torsades is the arrhythmia that is the main concern. It is potentially lethal, but often responds to magnesium and/or defibrillation. Cardioversion cam be used, if we can get the monitor to synchronize on the spiraling QRS complex, which is not as difficult as some would have us believe.
During the inclusion period between April 2009 and December 2009 a total number of 34 patients were analysed. All patients received mild therapeutic hypothermia treatment after resuscitation according to the current guidelines and regardless of the initial rhythm.
Out-of-hospital and initial in-hospital treatments were not altered for the study.
The target temperature of 33° C was maintained for 24 h. Intravenous sedation and analgesia were induced in all patients by a combination of midazolam (0.125 mg/kg/h) and fentanyl (0.002 mg/kg/h) with dose adjustment as needed. Muscle relaxation with repetitive administration of pancuronium (0.1 mg/kg) in order to prevent shivering was induced if necessary.
The interesting part is what they did when they saw these dramatically prolonged QT segments.
They did nothing. We need to learn to be a little less interventionist, when it comes to stable ventricular rhythms.
Post-resuscitation care was uninﬂuenced by the Holter ECG results and the ICU physicians followed the standard operating procedure for cardiac arrest patients. All patients completed the cooling procedure and survived the ﬁrst 48 h. Overcooling (central body temperature lower than 32° C) did not occur in any case, potassium serum levels were closely monitored and supplemented to stay within normal range and to avoid hypokalemia.
They did keep the potassium in the normal range, which is not something that patients always do outside of the hospital. This is one advantage these patients have over patients being treated for excited delirium, but this is what should be expected with admitted patients.
It isn’t clear if the doctors were blinded to the Holter results, or just did not act on anything they saw. I am interested in which it was.
The number of patients with at least one VT (ventricular tachycardia) was three (8.8%) during MTH and were non-sustained without any additional treatment. Torsade de pointes were not detected.
In spite of the very long QTc (median 564.47 ms), there were no cases of torsades. There were three cases of VT (≥ 30 seconds of ventricular ectopic beats), but all of these resolved spontaneously.
What happened to the good old days of having to panic and give the antiarrhythmic before the arrhythmia has a chance to go away on its own?
In one patient a maximum of 673.52 ms of QTc interval prolongation was reached after 12 h of 33° C as the highest recorded value without any additional drug treatment causing a QTc prolongation.
After 24 hours at 33°, the median QTc was 564.47 ms. A QTc longer than 450 is considered prolonged, but some will be comfortable well beyond that.
17 patients (50%) were discharged with a favourable neurological outcome (CPC 1–2) whereas 50% had an unfavourable outcome (CPC 3–5). The overall mortality rate was 38.2%,
An unfavorable outcome included both death and unfavorable neurological outcomes, so only 11.8% were discharged alive with unfavorable neurological outcomes.
Experimental data showed a stabilization of cell membranes during hypothermia and a higher likelihood of successful deﬁbrillation with a better ROSC rate in a swine model due to hypothermic conditions.9,10 This indicates that MTH lowers the incidence of arrhythmias rather than raising it. One should keep in mind that more profound hypothermia <30° will increase the risk and therefore temperature should be closely monitored in patients undergoing MTH.
Hypothermia does appear to protect against arrhythmia, but probably only when the hypothermia is mild.
The green line is at 450 ms, beyond which is considered to be a prolonged QTc.
The blue line is at 550 ms – a level that, if we are to believe those who are most concerned about QTc, is just begging for torsades. The patients’ rhythms should have changed to torsades long before they got to a QTc of 550 ms.
However, a QTc prolongation in elderly emergency patients (QTc ≥450 ms) has been observed in almost 544/1558 patients (35%) in a study by Seftchick et al. The most common comorbidities in this study were structural heart disease, renal failure, and stroke.14 Five percent of the patients with QTc prolongation died in the emergency department or during hospitalization but none had QTc prolongation or Torsade de pointes listed as a cause of death. Therefore a delay of repolarisation per se seems not necessarily torsadogenic.11
Will a prolonged QT segment cause torsades?
Maybe, but don’t bet on it, because thaere appear to be many more factors involved, than just the QTc.
 Severe QTc prolongation under mild hypothermia treatment and incidence of arrhythmias after cardiac arrest–a prospective study in 34 survivors with continuous Holter ECG.
Storm C, Hasper D, Nee J, Joerres A, Schefold JC, Kaufmann J, Roser M.
Resuscitation. 2011 Jul;82(7):859-62. Epub 2011 Mar 15.
PMID: 21482009 [PubMed - in process]
Controversial evidence & some reasoning.
Nitroglycerine is Contraindicated With Tachycardia?
- BP = Cardiac Output (CO) x Systemic Vascular Resistance
- CO = Stroke Volume x Heart Rate
An acute coronary event does not cause tachycardia. Tachycardia (without exertion) is almost always a result of decreased stroke volume. Stroke volume is dependant on venus return. So if stroke volume is down, and your body is trying to maintain normal cardiac output, so it may maintain a normal BP, the heart rate may be increased.
If the patient does not have pulmonary congestion (edema), nitro should be withheld if the patient is tachycardic. This is because the patient may be preload dependant as a result of dehydration, or some other hypovolemic condition. The tachycardia will most likely be compensatory, and the nitro will worsen the patients condition.
But anxiety can cause tachycardia…
Then console your patient and see if the tachycardia persists after they are calmed. If the tachycardia seems to accompany anxiety then nitrates may be acceptable. Be very weary of persistent tachycardia, whether they are anxious or not.
Patients Experiencing a Heart Attack Don’t Need O2?
Oxygen has recently shown to be much less benign a treatment than it was once thought to be. Hyperoxia leads to increased morbidity and mortality in stroke patients, post-arrest patients, head trauma patients, and it has most recently been discovered that hyperoxygenation may lead to poor outcomes in patients experiencing an AMI.
The answer isn’t so easy to understand. First of all, the research is still new. Just understand that these patients are not generally suffering from hypoxia. They are suffering from ischemic heart tissue, more specifically—myocardium. If their oxygen saturation is sufficient, than no additional O2 should be supplemented. Reasoning includes an elaborate explanation regarding free radicals. O2 is a free radical and may be toxic, leading to residual oxidative stress. This causes increased damage. Use of oxygen in MI patients questioned by new Cochrane review.
What is the Deal With Morphine?
Morphine is associated with an increase in morbidity when given to a patient experiencing an acute coronary event (an AMI).
Once again, there is no conclusive answer, but researchers from a CRUSADE study have three possible explanations.
- The first explanation is that patients treated with Morphine exhibit signs and symptoms of heart failure, and are treated as such. This isn’t really accepted as a plausible cause.
- The second, more widely accepted explanation is that Morphine masks symptoms of angina without correcting the underlined pathology. This means that caregivers may be less apt to provide follow-up treatments, procedures, and consults.
- The third explanation is that Morphine decreases the respiratory drive as well as causing CNS depression. Increased ischemia has been associated with these side effects, and extended infarction has been linked to Morphine itself.
|End point||No morphine
|Adjusted OR (95% CI)|
|Death (%)||4.7||5.5||1.48 (1.33-1.64)|
|Death or MI (%)||7.1||8.5||1.44 (1.34-1.56)|
|Postadmission MI (%)||3.0||3.8||1.34 (1.22-1.48)|
Morphine has bad effects when administered to patients with CHF.
Yes, it is in most prehospital guidelines as a recommended treatment for congestive heart failure. This will soon change…
The Acute Decompenstated Heart Failure National Registry (ADHERE) conducted a study on patients admitted with CHF who received morphine and yielded important results. There was a five-fold increase in mortality (13% versus 2.4%), a five-fold increase in need for intubation and ventilation (39.7% versus 14.4%), the intensive care unit admission rate was (15% versus 3.0%), and those patients who were admitted had a prolonged hospital stay (5.6 days versus 4.2 days). Although this was an observational study, it has had a major impact on the use of morphine for CHF patients. We know that morphine causes histamine release and subsequent hypotheses have been made concluding that this may increase catecholamine release. This may be the link to the poor outcomes. Additionally, there is a lack of evidence that morphine is related to any clinically significant preload reduction.
No More Intubations?
There has been a new paradigm shift in the way we think of resuscitation. This has brought with it, some new terminology—cardiocerebral resuscitation (CCR). CCR is meant to replace CPR, or cardiopulmonary resuscitation. The focus is shifting from the lungs, or pulmonary system, to the brain, or cerebrum.
There have been suggestions from the result of much research, advocating CCR for witnessed cardiac arrest, and CPR for primary respiratory arrest. This makes perfect sense, considering the pathologies. Overall though, there has been much more success when emphasis has been on chest compressions, as opposed to airway management.
Blind insertion, supraglotic airways are now rapidly finding their way into prehospital cardiac arrest guidelines throughout the country. The Combitube, Laryngeal Mask, and King LT/LTD are a few of the most common devices being utilized. The big sell, is the ability to insert these devices without any pauses in chest compressions.
This emphasis on chest compressions comes from research showing the need to prime the pump during the circulatory phase of cardiac arrest. This basically means that the heart and brain need to be perfused as good as possible up until defibrillation. Immediate defibrillation is only indicated within the electrical phase; which only lasts for approximately the first five minutes of pulselessness.
Despite the turmoil and mixed opinions about ETI in cardiac arrest, the evidence is clear—survival is better when the main focus is on adequate chest compressions. By taking the ETI aspect, and all of the complications that accompany it, out of the equation, resuscitation efforts consequently improve.
We haven’t even gone to the extreme yet. One study has shown that by simply placing a non-rebreather mask on a cardiac arrest victim and providing high-quality chest compressions, they increased neurologically intact survival rates from 15 to 39%.
Remember: Nearly all-medical research is flawed. This is one reason why medicine will remain ever changing. Fortunately the good evidence usually trumps the biased or bad evidence. No single study should change anything.
The History of Resuscitation Timeline
3000 BC – Mayan hieroglyphics and cave drawings indicate that they and the Peruvian Incas in South and Central America performed rectal fumigation to attempt resuscitation. This involves blowing hot air or smoke into the rectum of the casualty.
896 BC – “Then he got on the bed and lay upon the boy, mouth to mouth, eyes to eyes, hands to hands. As he stretched himself out upon him, the boy’s body grew warm.” (2 Kings 4:34)
1000 AD – A Muslim philosopher and physician known as Avicenna performed the first known experimental intubation of the trachea. Gold, silver, or other metals were used in an effort to support inspiration.
1500 AD – The Heat Method and flagellation were invented and tried. The heat method consisted of placing coals and hot ash onto the victim to counteract the cooling that death brings to the body. Flagellation involved whipping the patient to stimulate a response. These methods were both highly successful in awaking a deep sleeper, but futile resuscitative efforts.
1530 – The Bellows Method became very popular. This involved using a fireplace bellow to ventilate the patient. Unfortunately, airway anatomy was not very well known back then, and without hyperextension of the neck, the procedure didn’t work very well. However, modern day bag-valve masks were inspired by this archaic procedure.
1543 – Vesalius et al. published “De humani corporis fabrica”. This publication included descriptions of reviving animals by blowing into a tube.
1711 – For some reason, North American Indians and American colonists sought fit to bring back the rectal fumigation method. Lets hope, this was the final comeback tour for this procedure—for the patients, their families, and most of all, our sake.
1740 – The Paris Academy of Sciences made an official recommendation for mouth-to-mouth for the resuscitation of drowning victims. Of course it was the French who found benefit in placing their mouth on another’s.
1750 – Goodwin and Kite hypothesized that asphyxia caused the heart to stop; which was the ultimate cause of death. They theorized that electrical shock (defibrillation) should be used to restart the heart. Unfortunately this method was not appreciated because it required the victim be lain supine which caused the tongue to obstruct the airway.
1767 – The Society for the Recovery of Drowned Persons was founded and became the first organized group to take on sudden unexplained death. This was also the year that The Dutch Humane Society published their instructions for resuscitating drowning victims. They suggested keeping the victim warm, providing mouth-to-mouth, and once again, the dreaded rectal insufflations.
1770 – In Europe the leading cause of death at the time was drowning. The Inversion Method became widely used to treat cardiac arrests from drowning. This involved hanging the victim by his feet, often from a lifeguard tower. The pressure on the chest would force expiration while it was though the release of that pressure would stimulate inhalation. Lifeguards typically had to be pretty strong to lift the patients up and down repeatedly.
1773 – In an effort to provide artificial ventilation, the Barrel Method was invented. The rescuer would lay the victim prone over the length of a large barrel. He or she would then hold onto the patient by their feet and roll them back and forth.
1803 – The Russian Method was used, which may sound a lot like modern-day induced hypothermia. This entailed placing the victim’s body under a bed of snow or ice in an attempt to slow metabolism. Unfortunately, the brain was often left un-cooled, defeating the purpose.
1812 – Lifeguards became equipped with horses; which they kept tied to their lookout towers. The Trotting Horse Method utilized these horses when a drowning victim presented. The lifeguard would place the victim face down, draped over the horses back. The horse would then be led to a trot, up and down the beach. The bouncing of the victim’s chest on the horses back was thought to provide compression and relaxation. This was banned in 1815 when citizens complained that their beaches weren’t clean enough.
1849 – A student, M. Hoffa, was the first to witness and document the onset of ventricular fibrillation after inducing it with an electrical stimulus.
1856 – Dr. Marshall Hall challenged conventional wisdom at the time. He invented The Ready Method; which was aimed at providing artificial ventilation. The rescuer would roll the patient from a lateral position to the prone position about sixteen times a minute, with pauses to provide pressure while in the prone position to facilitate exhalation. This method was surprisingly successful for the time. An article from September of 1859 in the Editor’s Box of the British Medical Journal describes a physician’s use of the method to resuscitate a baby, after he had thought he delivered a stillborn.
1858- The Silvester Method was introduced in an effort to resuscitate stillborn children. The neonate would be laid supine and their arms would be lifted and then pressed against their chest. A rate of about sixteen arm lifts per minute was advocated.
1881 – Clara Barton founded the American Red Cross.
1891 – Dr. Friedrich Maass performed the first equivocally documented chest compression on a human being after John Howard wrote about the procedure.
1892 – French authors wrote about the Tongue Method. The victim’s mouth was held wide open while their tongue was rhythmically pulled back and forth.
1903 – It is reported that Dr. George Crile performed the first successful external chest compression to resuscitate a human. A year later he performed the first closed-chest cardiac massage in America.
1911 – The first edition of the Boy Scout handbook in the United States contained the Holger Nielsen Technique. The victim would be laid prone and their arms would be pulled on while pressure would be applied to their back.
1924 – Six cardiologists, representing several groups, founded the American Heart Association.
1932 – Dr. Frank C. Eve created his rocking method. This entailed using a stretcher with a patient laid on it, almost like a seesaw. It would be pivoted about its center in an effort to push the diaphragm alternately up then down. The Royal Navy adopted it during WWII for resuscitation of near-drowning victims.
1947 – Dr. Claude S. Beck, a thoracic surgeon for the University Hospitals in Cleveland, performed the first electrical defibrillation to save a human life.
1952 – Dr. Paul Zoll resuscitated two cardiac arrest patients in Boston by utilizing external defibrillation.
1956 – Peter Safer and James Elam invented mouth-to-mouth resuscitation; after identifying that expired air alone was sufficient enough to provide adequate oxygenation.
1957 – The United States Military adopted mouth-to-mouth resuscitation to revive unresponsive victims.
1960 – W.B. Kouwenhoven, J.R. Jude and G.G. Knickerbocker began to use what was termed Cardiopulmonary Resuscitation or CPR.
1966 – The National Academy of Sciences published a report entitled Accidental Death and Disability: The Neglected Disease of Modern Society, or “the white paper”. This placed pressure on the government to provide better ambulance services. This was the year the DOT took over prehospital education standards.
1973 – The American Heart Association and the American Red Cross began an aggressive campaign to teach and instill CPR methods. The rates and ratios have changed multiple times, but the fundamentals remained the same—ventilations and chest compressions.
1990 – The Chain of Survival became widely advertised by the AHA.
1996 – Emphasis was placed on early defibrillation.
2005 – AHA revisits basic life support, and places much more emphasis on chest compressions. Therapeutic hypothermia is listed in the AHA guidelines as a potentially beneficial treatment for revived cardiac arrest victims.
Now – Cardiocerbral Resuscitation, or CCR de-emphasizes airway management, and reinforces AHA’s recommendations for better chest compressions. The impedance threshold device has shown to improve cardiac and cerebral perfusion during CPR. Evidence supports the transportation of revived cardiac arrest patients to a PCI-capable facility.
Chronicles of EMS, A Seat at the Table takes on CPR effectiveness. The Las Vegas video that they mention can be found below as well. Keep up the good work Justin and Mark!
Side note – ILCOR, The International Liaison Committee On Resuscitation has not found any supporting evidence for the Autopulse. They are the ones whom do the research for AHA. Also, transporting patients without a pulse should be re-looked at by any agency performing this practice. The initial treatment at the ER will not differ from the treatment we provide at the scene per ACLS guidelines. Why not give the patient the best chance possible. If they don’t get a pulse back on scene, it is probably never going to come back–that’s just the facts.
It’s that time again. As most of us Americans in the wide world of emergency medicine know, every five years the American Heart Association updates their recommendations. Those recommendations happen to be the standard for most prehospital agencies, and hospital systems. They say and we do. So what are we going to be doing now?
This year should not be bringing about any mega changes. The direction has stayed the same for the most part.
Where do the updates come from?
ILCOR – The International Liaison Committee on Resuscitation
Process for Evidence Evaluation
The publication of the 2010 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) Science with Treatment Recommendations (CoSTR) will represent the scientific consensus of experts from a variety of countries, cultures and disciplines. Internationally recognized experts were brought together by the International Liaison Committee on Resuscitation (ILCOR) to evaluate and form an expert consensus on all peer reviewed scientific studies related to CPR.
To achieve this goals, ILCOR is conducting systematic reviews and updates of scientific evidence supporting resuscitation treatment recommendations. More than 500 resuscitation scientific topics will undergo evidence-based review. This process represents the most comprehensive, systematic review of the resuscitation literature to date.
The worksheets posted at this site represent the first step of an international consensus evidence evaluation process that will culminate in the publication of the 2010 International Consensus on CPR and ECC Science with Treatment Recommendations. In addition, resuscitation council-specific guidelines will also be published based on this international science consensus. Worksheet authors and expert reviewers worked very hard to present the information objectively.
The information contained in these worksheets will be presented and discussed between now and early 2010. In early 2010, the International CPR Consensus Conference will convene to allow final presentation and discussion of these worksheets, leading to evaluation and consensus by respective ILCOR Task Forces.
Readers are cautioned that these worksheets are a preliminary review and do not represent any ILCOR Task Force or Resuscitation Council recommendations.
ILCOR recognizes that the integrity of the evidence evaluation process depends on successfully managing real and perceived conflict of interest. ILCOR has policies in place to manage conflict of interest.
The 2010 evidence evaluation and science review process will culminate with the International CoSTR Conference in early 2010, in Dallas, Texas.
A separate publication covering guideline recommendations will be published by each resuscitation council.
So what does this all mean?
The AHA is part of an international committee that uses a systematic review system to scan through all the most valuable research available. The research is graded by how useful an unbiased it is, and then recommendations are made based upon a compilation of the results. The package all of this up in a nice-looking book, packed with a bunch of fancy flow charts, tables, and algorithms, and we buy it.
Time of old
Amiodarone – Back in 2000 Amiodarone was given a class IIb recommendation from AHA. This was a push from, who else, the manufacturers of Amio. This happened synchronously with the changing of Lidocaine from a class IIb to an indeterminate rating. This occurred after a study showed that Amiodarone improved the number of cardiac arrest that regained pulses. This was accepted by many, and all the better, Amio works in atrial and ventricular arrhythmias–yippee.
So does this mean we are going back to lidocaine? Not sure, because there isn’t any evidence that lidocaine is any better either–should we confuse everyone more? In fact, there is no evidence that any dysrhythmic does anything beneficial in cardiac arrest. That’s right, no quality evidence supporting beneficial effects of dysrhythmics. Want some more? NO DRUGS administered in cardiac arrest have any supporting evidence!
Olasveengen TM, Sunde K, Brunborg C, et al. Intravenous drug administration
during out-of-hospital cardiac arrest. JAMA 2009;302:2222-2229.
Despite the traditional use of intravenous medications such as vasopressors and antiarrhythmics for victims of cardiac arrest, there is actually very little evidence to support these therapies. On the contrary, a recent multicenter center study demonstrated that the use of intravenous medications that are advocated in standard advanced cardiac life support (ACLS) guidelines was ineffective at improving survival of patients with out- of-hospital cardiac arrest (1). Olasveengen and colleagues now add further support to the contention that the use of intravenous medications in victims of non-traumatic cardiac arrest is not associated with improvements in meaningful outcomes. The authors performed a prospective randomized trial of consecutive adults with non-traumatic cardiac arrest that were treated within their emergency medical services (EMS) system in Oslo between 2003 2008. Patients were randomized to either receive standard ACLS therapies with intravenous drug administration (IV group) or ACLS therapies without any intravenous drugs (no IV group). A total of 851 patients were included in the study, 418 patients in the IV group and 433 in the no IV group. The researchers found there was an increase in survival to hospital admission with return of spontaneous circulation in the IV group vs. the no IV group (32% vs. 21%, P < 0.001). However, there was no difference between the IV group vs. the no IV group in terms of survival to hospital discharge (10.5% vs. 9.2%, P = 0.61), survival with favorable neurological outcome (9.8% vs. 8.1%, P = 0.45), or survival at 1 year (10% vs. 8%, P = 0.53). The results demonstrate that with the use of IV ACLS medications, patients simply die in the hospital rather than in the ED. Practically speaking, this amounts to increased intensive care unit bed utilization, hospital resource utilization, and expenses; but without any increase in meaningful survival. In this era of ED and hospital overcrowding and the increasing demand for cost-effectiveness in medical therapies, Stiell’s and Olasveengen’s studies should force us to consider that the use of IV medications for patients in cardiac arrest should be the exception rather than the rule…or guideline.
1. Stiell IG, Wells GA, Field B, et al. Ontario Prehospital Advanced Life Support Study Group. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med 2004;351:647-656.
Back to Amiodarone 2010:
CONSENSUS ON SCIENCE:
Evidence from 1 RCT demonstrates the benefit of amiodarone over placebo for shock refractory or recurrent VT/VF for the endpoint of survival to hospital admission, but not to survival to hospital discharge. Retrospective trials show that lidocaine may be more beneficial than placebo, but selection bias mars these trials. In trials that directly compare amiodarone to lidocaine, patients administered amiodarone generally do better in short term results (ie survival to hospital admission), but no trial has shown an improvement in overall survival (Dorian P 2002 p884, Somberg J 2002 p853).
These trials were performed before the benefits of hypothermia was known, thus they did not incorporate this now proven therapy which improves survival after ROSC. Whether survival to hospital discharge and neurologic survival could be improved with amiodarone and subsequent hypothermia is not known. If that is the case then a stronger argument for amiodarone could be made; if that is not the case then an argument could be made to not give an AAD at all.
CPR Before Defibrillation
It was taught, back in 2005 by AHA, that we need to prime the pump. It was theorized that performing early defibrillation has no benefit because the heart was not being adequately perfused. This lead to a 2 minutes of CPR prior to shocking in an unwitnessed arrest rule. This is what we, who are AHA compliant, are doing.
CONSENSUS ON SCIENCE:
Two randomized controlled trials (LOE I) (Baker 2008 p424; Jacobs 2005 p39) demonstrated no improvement in ROSC or survival to hospital discharge in patients suffering out-of-hospital VF or pulseless VT who received CPR by EMS personnel for a period of 1.5 to 3 minutes before defibrillation, regardless of EMS response interval being greater or less than 5 minutes. One case series study (LOE IV) (Campbell 2007 p229) also failed to demonstrate improvements in ROSC or survival to hospital discharge with bystander versus no bystander CPR before defibrillation.
One randomized controlled trial (LOE I) (Wik 2003 p1389) and clinical trial (LOE III) (Cobb 1999 p1182) identified overall similar findings however improvements in ROSC, survival to hospital discharge and neurological outcome were observed in patients where the EMS response interval was greater than 4 to 5 minutes.
Evidence from one LOE 1 study (Wik 2003, 1389), one LOE 3 study (Cobb 1999, 1182) and five LOE 5 studies (Berg 2004, 1352; Kolarova 2003, 2022; Menegazzi 1993, 235; Menegazzi 2004, 926; Niemann 1992, 281) support the strategy to delay defibrillation to give BLS first for 1,5 to 8 minutes, in particular when the delay to ambulance arrival exceeds 5 minutes and no BLS is given before ambulance arrival. Evidence from two LOE 1 studies (Baker 2008, 424; Jacobs 2005, 39), one LOE 3 study (Campbell 2007, 229) and nine LOE 5 studies (Berg 2004, 1352; Yakaitis 1980, 157; Menegazzi 2003, 261; Menegazzi 2000, 31; Seaberg 2001, 301; Kolarova 2003, 2022; Niemann 2000, 543; Menegazzi 1993, 235; Rittenberger 2008, 155) do not support this strategy and are neutral. One LOE 5 study (Indik 2009, 179) gave direct evidence for the opposite strategy
Level of evidence – all that LOE stuff you see above is a reference to the grade the mentioned study received by the reviewer.
Randomised Controlled Trials:
These studies prospectively collect data, and randomly allocate the patients to intervention or control groups.
Studies using concurrent controls without true randomisation:
These studies can be:
· experimental – having patients that are allocated to intervention or control groups concurrently, but in a non-random fashion (including pseudo-randomisation: eg. alternate days, day of week etc), or
· observational – including cohort and case control studies
A meta-analysis of these types of studies is also allocated a LOE = 2.
Studies using retrospective controls:
These studies use control patients that have been selected from a previous period in time to the intervention group.
Case series: A single group of people exposed to the intervention (factor under study), but without a control group.
As with other categories of Levels of Evidence, we have used LOE 5 to refer to studies that are not directly related to the specific patient/population. These could be different patients/population, or animal models, and could include high quality studies (including RCTs).
So according to the evidence, we may need more evidence. However, there isn’t much support to the current guidelines. Once again, do we change this back and confuse more people when we are uncertain if outcomes will improve?
Cardiocerberal Resuscitation or Cardiopulmonary Resuscitation?
Should EMS be doing chest compression only CPR? This is a good question when considering primary cardiac arrest. We know that primary respiratory arrest should involve aggressive airway management.
CONSENSUS ON SCIENCE
Six fair to good LOE 5 animal studies (Berg 1993, 1907; Berg 1997, 1635; Berg 2001, 2464; Ewy 2007, 2525; Kern 1998, 179; Kern 2002, 645) have shown comparable or better outcomes with continuous chest compression CPR as compared with interrupted compressions for ventilation in nonasphyxial cardiac arrest and in concept support such a change in resuscitation strategy. However animal models do not necessarily mimic the anatomical or arrest features of humans, and for these reasons arguably may be less applicable to human resuscitation. Clinical evidence from three retrospective cohort LOE 3 studies in adults suffering from cardiac arrest (Bobrow 2007, 1158; Kellum 2006, 335; Kellum 2008, 244) showed that provision of chest compressions in the absence of rescue breathing by trained professional (EMS) providers led to an improvement in survival to hospital discharge compared to provision of chest compressions with rescue breathing. However, these studies had methodological shortcomings that limit the ability to determine whether the improvements in survival were attributable to the provision of chest compression-only CPR in the absence of rescue breathing, including the lack of randomization, the implementation of other resuscitation protocol changes that may have affected outcomes, or simply a stronger clinical emphasis on the provision of good CPR. The remainder of clinical studies addressing this issue evaluated the outcome from continuous chest compression versus interposed ventilation CPR by untrained laypersons (bystander CPR),and did not directly address provision of care by trained professionals.
So there are studies out there, just maybe not enough–once again. There is also research on different compression:ventilation ratios showing promising data. Guess we will find out what really happens in October.
More of the same
There is a lot more evidence out there advocating chest compressions. No pulse checks, just compressions. More and more compressions. Push hard and push fast. Good chest compressions. Are you getting all of this?
Therapeutic hypothermia is gaining more popularity. The evidence is outstanding.
CONSENSUS ON SCIENCE:
Who to cool?
Evidence from one good randomized trial (LOE 1) (HACA, 2002, 549) and a pseudo-randomised trial (LOE 2) (Bernard, 2002,557) demonstrate improvement in neurological outcome after discharge from hospital in patients who had an out-of-hospital VF cardiac arrest, who were still comatose, and who were cooled within minutes to hours after return of spontaneous circulation to 32-34ºC for 12-24 hours. Two studies with historical control groups (LOE 3) showed improvement in neurological outcome after therapeutic hypothermia for comatose survivors of VF cardiac arrest (Belliard, 2007, 252; Castrejon, 2009, 733) One small (n = 30) randomized trial (LOE 1) showed reduced plasma lactate values and oxygen extraction ratios in a group (n =16) of comatose survivors after cardiac arrest with asystole or PEA who were cooled with a cooling cap (Hachimi-Idrissi, 2001, 275). Six studies with historical control groups (LOE 3) showed benefit after therapeutic hypothermia in comatose survivors of OHCA after all rhythm arrests (Bernard, 2007, 146; Oddo, 2006, 1865; Busch, 2006, 1277; Sunde, 2007, 29; Storm, 2008, R78; Don, 2009 3062). One studies with historical controls showed better neurological outcome after VF cardiac arrest but no difference after cardiac arrest from other rhythms (Bro-Jeppesen, 2009, 171). Two non-randomised studies with concurrent controls (Arrich, 2007, 1041; Holzer, 2006, 1792) indicate possible benefit of hypothermia following cardiac arrest from other initial rhythms in- and outof-hospital.
How to cool?
Nine case series (LOE 4) indicate that cooling can be initiated safely with intravenous ice-cold fluids (30 ml/kg of saline 0.9% or Ringer’s lactate) (Kliegel, 2005, 347; Kliegel 2007, 56; Bernard, 2003, 9; Virkkunen, 2004, 299; Kim, 2005, 715 ; Jacobshagen, 2009; Kilgannon, 2008; Spiel, 2009; Larsson, 2010;). Two randomised controlled trials (Kim, 2007, 3064; Kamarainen, 2009, 900), one study with concurrent controls (LOE 2: Hammer, 2009, 570) and three cases series (LOE 3) (Kamarainen,2008, 360;Kamarainen, 2008, 205) indicate that cooling with IV cold saline can be initiated in the pre-hospital phase.
More For Post-Arrest
There is evidence that patients who are resuscitated from primary cardiac arrest should be immediately cathed.
The significance of this new literature cannot be overstated. If further studies confirm these findings, it would strongly argue for enormous changes in prehospital systems of care to recommend that all survivors of primary cardiac arrest should be immediately transported to hospitals that have the capability of performing urgent PCI in conjunction with therapeutic hypothermia. Based on the current literature, it certainly seems advisable that emergency health care practitioners that care for resuscitated victims of primary cardiac arrest should engage in conversations with cardiology consultants and urge them to take an aggressive approach to PCI in these patients.
What does this mean for us? Post-arrest 12-lead ECGs for now. In the future, this may mean that we bypass non-PCI facilities with our post-arrest patients. If you think this will last long, you are wrong. Post-arrest patients are high dollar patients. Just think about all of the work-ups done on these patients. Don’t think that the non-PCI hospitals won’t be rushing to find a way around this. Will this mean more PCI centers? Probably not, because all of the other cardio-intervention seeking patients end up with big medical bills too–but who knows.
So even though AHA came out and said that their initial recommendation for biphasic defibrillators is not backed by any evidence, there may be an actual benefit to having them. There is evidence supporting what I am about to tell you, but it may not make it into the 2010 update. I think it will though. It goes against what we have all learned. Remember “I’m clear, you’re clear, we’re all clear!”
There is no harm to a rescuer performing chest compressions, when defibrillation is performed using a biphasic monitor.
That’s right. It has been said that more electricity passes through your body on one of those scales that checks your BMI than touching a patient when they are getting shocked. It has to be a biphasic defibrillator though.
So that’s all so far. Go scan through the worksheets if you’d like. There is a ton of good research available. We can only assume, as of yet, what the final recommendations will be.
Allow me to introduce myself. My name is Chris Kaiser, or Ckemtp, and I write the EMS blog http://www.lifeunderthelights.com/ – I am a Nationally Registered Paramedic holding licensure in Illinois, Iowa, and also in Wisconsin. A few months ago I was asked to become a contributor to write for this blog and I jumped at the chance to intermingle my stuff with the venerable names here. Unfortunately, it has taken me a while to get something up here with the work needed to move from my old site to the new site. Today I’m fixing that and I would like to repost this article here with a few updates. I hope you find it educational.
Visitors to my blog probably know that at my ambulance service we tend to bring back a lot of codes. I talk about it a lot. Back in 2004 our medical director, Dr. Michael Kellum, got us involved in a “Demonstration Project” to bring Continuous Compression CPR or Cardiocerebral resuscitation to a rural area. Since that time, the results have been more than dramatic. Depending on what statistics you look at, we may be “Saving” almost 50% of witnessed arrests found to be in ventricular fibrillation.
It’s all explained at http://www.callandpump.org/, but if you want to go right to the whitepaper that explains what we do, why we do it, and how it’s done then you want to go here: http://callandpump.org/assets/Proposal_Current.pdf – This link is explains the demonstration project initiated by Dr. Kellum et al. in the two county area that I work in. This paper was published in 2004 at the beginning of the project.
This is a link to the results published in the Annals of Emergenc Medicine in 2008 – http://www.ncbi.nlm.nih.gov/pubmed/18374452?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
You may be interested in this part:
“RESULTS: In the 3 years preceding the change in protocol, there were 92 witnessed arrests with an initially shockable rhythm. Eighteen patients survived (20%) and 14 (15%) were neurologically intact. During the 3 years after implementation of the new protocol, there were 89 such patients. Forty-two (47%) survived and 35 (39%) were neurologically intact. CONCLUSION: In adult patients with a witnessed cardiac arrest and an initially shockable rhythm, implementation of an out-of-hospital treatment protocol based on the principles of cardiocerebral resuscitation was associated with a dramatic improvement in neurologically intact survival.”
This is good stuff. Remember, the above is only reflective of those included in the study, who are “Witnessed arrest(s) with an initially shockable rhythm”. Anecdotally, I’ve personally attended those that were not in a shockable rhythm and witnessed greater effectiveness as well.
Here’s the short version of our protocols for Witnessed V-Fib Arrest: (and for those of you who want more, email me at: firstname.lastname@example.org and I will be happy to send you a copy of the protocols)
We follow an acronym called MCMAID in our resuscitation protocols, it stands for:
Metronome – We carry a metronome in our monitor/defibrillator bags that clicks out at 100 beats per minute. We are to compress at 100bpm. No more, no less. This metronome keeps us on rhythm and reminds us to be on the chest.
Compressions – 100 compressions per minute. Do not stop. Initially, we are to administer 200 compressions (2 minutes) before our first shock. We are to limit any interruptions in compressions absolutely as much as possible, charging our defibrillators while compressions are ongoing and recognizing V-fib through the compressions if possible. Compress hard and deep, completely releasing tension on the chest upon recoil to maximize the compression and decompression of the chest.
Monitor – Place the monitor on the patient using fast patches. Do not stop the 200 compression cycles to determine the rhythm. Shock at max joules biphasic. If you can anticipate V-Fib, charge the defib during the compressions and only stop long enough to clear for the shock. Don’t check the pulse, get right back to compressions.
Airway – Initially, a BLS airway will be placed in the patient and a non-rebreather oxygen mask will be placed on the patient. If the airway must be controlled by more advanced means to protect and ensure a patent airway, now is the time to do so.
Intravenous Access – Most of the time, this is accomplished through the means of the Ez-IO drill that we carry and love. (See: Alternative Circulatory Access Strategies – Hi Ho IO) This can also be obtained through peripheral or EJ IV access.
Drugs – Epinephrine 1:10,000 1mg IVasopression 40 IU, Amiodarone 300mg, then Epinephrine 1:10,000 1mg q 3-5min. If refractory, we may give an additional 150mg Amiodarone IV.
Dr. Kellum came down again for our monthly training recently and let us know the latest breakthroughs and orders in the project. He is stressing the importance of End-Tidal CO2 (ETCO2) monitoring and states that no pulse check is necessary without a spontaneous increase in ETCO2. He expects every intubated (or combitubed) patient to have ETCO2 monitoring in place.
He also expects that we will monitor ETCO2 readings as a way to prove effectiveness of compressions. Rescuers who cannot get ETCO2 readings consistent with other personnel when providing compressions shouldn’t be doing compressions.
Rescuers should switch off compressions EVERY ONE MINUTE whenever possible. This is providing some fantastic results in preliminary trials.
He also stated that the effectiveness of the CCR protocols are showing a marked increase in refractory V-fib. He hinted that the protocols might soon show a need for thrombolytic use in treatment of refractory V-Fib.
Stay tuned folks, I am happy as heck to be included in this. I will bring updates, with permission, as many times as I get them. You can find more information on this on http://www.lifeunderthelights.com/. It’s truly exciting stuff.
Again returning to the EMS Garage post with Mickey S. Eisenberg, MD on resuscitation, the rest of the episode was great. One of the points brought up was, at about 52 minutes in, Buck Feris mentions a quality assessment/improvement method in a system, that has a supervisor respond to debrief the crew after every arrest. Reviewing what went right and what went wrong.
Dr. Mickey S. Eisenberg earlier had talked about methods of improving outcome and the approach of reviewing every unsuccessful resuscitation by asking, Why wasn’t this patient resuscitated?
These are excellent approaches. If we are not reviewing our calls, how do we expect to improve? I think that both of these approaches are still too limited. We should review all calls that fall into certain categories. For example, all cardiac/potentially cardiac calls, all respiratory calls, all calls involving any level of pain, et cetera. Maybe not right after the call, but as soon as is practical.
In my opinion, people who are opposed to continually improving patient care are not needed in EMS.
What kind of ignorance is needed to claim that we should not be improving our care of patients? Real medicine is about continually improving patient care.
Dr. Eisenberg goes on to make an essential point about a method used to improve quality. Audio recordings of cardiac arrests by the defibrillator. He states,
We have found that immensely valuable. We’ve used it in our system from day one. We’ve recorded virtually every cardiac arrest event, with not only the rhythm, but with the voice. That has been a very valuable tool, to reconstruct for educational purposes, what exactly was going on in the resuscitation and when. Because, without it you can’t really tell when there are gaps in CPR, you can’t even tell when ventilations are occurring, you can’t tell reasons why there was the delay in this or that.
And if it’s done for the purpose of education and never for the purposes of discipline. We’ve never, ever, used these tapes for disciplinary reasons. They’ve always been used for education. You can learn an awful lot, and begin to piece together what went on.
If we want to improve quality, we need to make it safe for people to bring up and discuss mistakes. If the employees are afraid of punishment for raising concerns about things that went wrong, we will never learn about many of the problems in the system. We need more people in EMS, who understand this.
Again, in my opinion, people who are opposed to continually improving patient care are not needed in EMS.
A cooperative broadcast between EMS Garage (above) and EMS EduCast (below):
Back to the EMS Garage post with Mickey S. Eisenberg, MD on resuscitation, the rest of the episode was great. One of the points brought up was, How do we strengthen the first links in the Chain of Survival?
Without the right start, how can we expect the later parts to be effective?
But we do.
We expect that this is all about paramedics, ACLS (Advanced Cardiac Life Support), EDs (Emergency Departments), drugs, and invasive procedures.
So, why have the Chain of Survival?
Because the stuff at the end, if it works at all depends on the stuff at the beginning. You do not put an egg and some cheese on a plate and declare that it is an omelette. The preparation is important.
Dr. Eisenberg addressed some of the questions that almost everybody else
runs away from, while screaming obscenities ignores.
What are the best investments of money to improve resuscitation?
Do we need to have the public go through an entire AHA/ARC CPR course, or can we provide the level of education needed to meet the needs of the patient by other means?
I wrote about this subject a bit before, in EMS Garage, CPR, Continuous Compressions, and Resuscitation. A link to a video that is not viewed enough (only a little over 2,000 total views listed by YouTube) was sent by Buck Feris. This video is an example of what we need to be using much more.
We need to get the attention of the people who might be in a position to perform CPR. Not the ones taking a course, because of a job requirement. They are a captive audience, and sometimes we make them feel exactly that way. That is not the right approach.
What is wrong with shorter courses, distance courses, and public service spots?
Do we need to delude ourselves that CPR is rocket science?
experience sudden cardiac arrest die in the area where Dr. Eisenberg has been improving resuscitation, you have almost a 50/50 chance of resuscitation. This is probably in large part due to the use of alternative educational methods to encourage by-standers to do CPR.
Or we could keep making excuses.
A cooperative broadcast between EMS Garage (above) and EMS EduCast (below):
Although I link to this article, there is something that I observed that is disappointing. There is only one mention of Dr. Eisenberg in the article, and that is a footnote. An article he wrote in 1985. Just because I am curious, I decided to see how many papers I could find by Dr. Eisenber in a PubMed search. For the most recent paper, I have to go all the way back to October of 2009 – we aren’t even there, yet. Going almost 150 articles further – to Staphylococcal food poisoning aboard a commercial aircraft from the Lancet, which was awarded the 1975 Alexander D. Langmuir prize by the Center for Disease Control. Wikipedia, you are missing a lot. More than a minor omission.
Then there is Dr. Eisenberg’s new book:
Resuscitate!: How Your Community Can Improve Survival from Sudden Cardiac Arrest
By Mickey S. Eisenberg, MD
Amazon.com link with a good video review by Greg Friese.