Cross-posted to the Prehospital 12-Lead ECG blog.
Here is an interesting case submitted by Billy Eskridge.
EMS is called to an assisted living facility to evaluate a 94 year old female complaining of chest pain.
History of present illness:
Approximately 1 hour prior to EMS arrival, the patient had complained of a headache. A nurse gave the patient a Lortab. About 15 minutes later the patient started complaining of chest discomfort.
The nurse gave the patient two 0.4 mg NTG tablets over 20 minutes with no relief of the chest pain. The patient requested to be seen by a physician.
Patient is slightly confused and lethargic but states that she feels "sick all over." The nurse states this is unusual for the patient.
Past medical history:
Complex medical history including hypertension, aortic stenosis, and mitral regurgitation
SpO2: 85 on RA
The cardiac monitor is attached.
A 12-lead ECG is captured.
Here are the computer measurements and interpretive statements.
Billy Eskridge asks the following questions:
Since this patient has an internal pacemaker and wide QRS complexes, is it possible to identify the ST/T changes of ischemia or acute injury?
I have also observed that not every beat is paced, and that there are come supraventricular beats which are also wide complex, showing a LBBB.
I know that there are certain tricks for diagnosing acute MI in LBBB, but I'm not familiar with them.
I am also aware that normal ST changes in wide complex rhythms can be used for diagnosis of MI if an old 12 lead is available to compare the current one to, but is this valid for both paced and supraventricular rhythms with a BBB?
If this rhythm was paces every beat without any apparent conduction abnormality can you scan it for AMI?
In the first place, even though the pacing spikes seem to "disappear" occasionally in the rhythm strip, it shows 100% pacing. I suspect that the pacing spikes are simply lining up perfectly with the lines on the graph paper, but regardless, we can rest assured that it's 100% paced because there is no change whatsoever in the R-R interval or QRS morphology.
In this case, the 12-lead ECG shows a fairly typical looking paced rhythm consistent with a pacing lead in the apex of the right ventricle. Namely, it shows LBBB morphology in lead V1 with a left axis deviation. It also shows negative concordance in the precordial leads, which is a common finding with paced rhythms.
You will note that the ST-segments and T-wave are deflected opposite the main deflection of the QRS complex (which is also the terminal deflection of the QRS complex). This is consistent with a "normal" paced rhythm and the "rule of appropriate T-wave (and ST-segment) discordance" with LBBB or paced rhythm.
Another important finding is that the larger the QRS complex, the more pronounced the secondary ST-T wave abnormality in the opposite direction. This is also true with strain patterns with left ventricular hypertrophy (LVH).
However, there are limits as to the expected amount of discordant ST-segment elevation in the presence of LBBB or paced rhythm.
According to Sgarbossa's Criteria, discordant ST-elevation (that's ST-elevation that is opposite the main deflection of the QRS complex -- in other words, ST-elevation in a lead with a negative QRS complex) > 5 mm is suggestive of AMI.
The problem is that QRS complexes with extremely deep QRS complexes will show more ST-elevation, and that's normal for LBBB and paced rhythm. For example, if you have a QRS complex in the right precordial leads with an S-wave that is 50 mm deep, you can have 5 mm of discordant ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine.
Dr. Smith and colleagues from Hennepin County Medical Center propose a modified rule for discordant ST-elevation where you look for discordant ST-elevation that is 0.25 (or 1/4) the depth of the QRS complex.
Regardless, this 12-lead ECG shows a normal looking paced rhythm with appropriate T-wave discordance and ST-segments that are normal looking within the context of paced rhythms.
To learn more about Sgarbossa's Criteria and the "rule of appropriate T-wave discordance" see these previous posts:
Identifying AMI in the presence of LBBB - Sgarbossa's Critera - Part I
Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part II
Tom B | 11:22 AM | | 2 comments
Cross-posted to the Prehospital 12-Lead ECG blog.
This study has received a lot of attention. I will interchangeably use the terms the IV (IntraVenous) group and the epinephrine group depending on the terminology I think is more relevant at the time. The distinction is not one that I believe is important. This is a study of IV medication in cardiac arrest. Epinephrine is the stated focus of the study.
There has never been any evidence to suggest that medication leads improved resuscitation outcomes. Unless your idea of an improved resuscitation outcome has nothing to do with quality of life.
Beneficial short-term effects of epinephrine have been shown in animal studies,3-5 but there is increasing concern for increased myocardial dysfunction6,7 and disturbed cerebral microcirculation after cardiac arrest.8
Some people argue that the short-term effects are important. If we do not get a pulse back, we will not resuscitate anyone. This is true, but the problem is how much long-term damage do we inflict just to obtain that short-term improvement?
High-dose epinephrine is no longer recommended, even though it was better than standard-dose epinephrine at producing ROSC (Return Of Spontaneous Circulation). The current recommendation for epinephrine is based on this same misconception. More ROSC = better outcomes - except that the dogma is not supported by any evidence.
CONCLUSIONS--High-dose epinephrine (HDE) significantly improves the rate of return of spontaneous circulation and hospital admission in patients who are in prehospital cardiac arrest without increasing complications. However, the increase in hospital discharge rate is not statistically significant, and no significant trend could be determined for neurological outcome. No benefit of NE compared with HDE was identified. Further study is needed to determine the optimal role of epinephrine in prehospital cardiac arrest.
That study was 17 years ago. That was far from the first study of epinephrine. There has been many studies of epinephrine in cardiac arrest since then.
We still do not have any research to show improved outcomes with any dose of epinephrine to treat cardiac arrest, but rather than admit that epinephrine should only be used in well controlled studies, we continue to make excuses. We are practicing alternative medicine, not real medicine.
Absence of evidence of benefit does not mean an absence of benefit, but when does it become enough evidence to insist that we stop using this ineffective and potentially harmful drug as the standard treatment?
Back to the current study.
Because there are no randomized controlled studies showing improved survival to hospital discharge with any drugs routinely administered during CPR, we concluded such a study was warranted.
This study is possible because these researchers are outside of the US. In the US, the IRBs (Institutional Review Boards) seem to have concluded that it is unethical to deviate from the standard treatment, even if the standard treatment is harmful. Of course, we can never learn if the standard treatment is harmful, or even if it is beneficial, if we are prohibited from studying the treatment. However, the IRBs' definition of ethics seems to have been arrived at while consuming hallucinogens and reading Lewis Carroll.
Epinephrine in cardiac arrest is also firmly established outside of the US. Here is a part of their explanation of the study design.
In this prospective, randomized controlled trial of intravenous drug administration during out-of-hospital cardiac arrest, we compared outcomes for patients receiving standard ACLS with intravenous drug administration (control) and patients receiving ACLS without intravenous drug administration (intervention).
ACLS is Advanced Cardiac Life Support - almost all of the treatments that would be given in the ED (Emergency Department). Not giving the drug is the intervention. Giving the drug is considered the non-intervention - the control against the effects of the treatment, which is the non-treatment.
Defibrillation was attempted in more patients in the intravenous group compared with the no intravenous group (47% vs 37%, respectively; OR, 1.16 [95% CI, 0.74-1.82]). More defibrillation shocks were delivered to those who received defibrillation in the intravenous group compared with the no intravenous group (median, 3 [range, 1-22] vs 2 [range, 1-26], respectively; P = .008). Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table1).
While there were no apparent differences in the quality of CPR, the more frequent defibrillations might be worth looking at. One of the important aspects of this study, as opposed to most prehospital research, is the recognition of a need to control for quality.
The explanation for the more frequent defibrillations that seems most likely is that the epinephrine produced a shockable rhythm more often than CPR alone produced a shockable rhythm. Since a shockable rhythm appears to be the next best thing to ROSC, this would not be a surprise. Many patients will change from a shockable rhythm to asystole when defibrillated. Defibrillation is a profound vagal stimulus and asystole is the ultimate vagal state. Even with similar initial rates of shockable rhythms, some of both groups would be expected to be shocked into asystole. The epinephrine, being a huge cardiac stimulus, would be expected to lead to a return of a shockable rhythm more often than just CPR. In other words, if the epinephrine is expected to produce ROSC more often, it should also produce a shockable rhythm more often. The authors came to a similar conclusion.
Without differences in the predefined primary outcome, patients in the intravenous group received more defibrillations, were resuscitated for a longer period, and more frequently had ROSC. With similar and adequate CPR quality, this is likely due to the pharmacological effects of the drugs used (epinephrine, atropine, and/or amiodarone). This finding is consistent with previous animal studies with epinephrine,6,7 and clinical studies evaluating the effects of amiodarone,23 atropine,24 and even high-dose epinephrine,25 all of which documented improved short-term effects without improving long-term outcomes.
One major criticism of the methods is that they did not have a placebo to be given to keep the EMS crews blinded to the actual treatment. The authors do admit that this is a limitation. Of course, this placebo would probably not be called a placebo, since the epinephrine arm is the placebo arm, while the non-treatment arm is the active intervention arm, but that is really only an amusing problem of terminology and attitude. When the epinephrine group is the group with an IV line in place during resuscitation and the no epinephrine group is the one that does not have an IV until after return of pulses, there is not even an attempt at blinding. Did this lead to any detectable difference in the way patients were treated by EMS, other than other than the differences intended by the study design?
Our study has several limitations. First, ambulance personnel could not be blinded to the randomization. Closely related to this, only patients who were randomized to the no intravenous group could be monitored with regard to protocol compliance. If intravenous drugs were administered to a patient in the no intravenous group, violation of the study protocol could be
documented. If intravenous drugs were not administered to a patient in the intravenous group, several valid reasons could exist, such as rapid ROSC. We have no reason to believe that personnel refrained from establishing intravenous access under the pretense that the procedure was unsuccessful. The ambulance personnel involved were strongly committed to testing the hypothesis presented, but we cannot totally rule out possible bias toward procedures such as intravenous access and administration of drugs, which have been important in Norwegian culture for decades.
This is a reason for creating a sham drug to use for the study. Without knowledge of the contents of the syringes being used, any bias of the treating medics should not affect the results. That is the purpose of blinding.
Analysis was performed on an intention-to-treat basis regardless of which treatment was actually given.
In the No IV group, 10% received IV drugs. 9% of patients received epinephrine.
In the IV group, 82% received IV drugs. 79% of patients received epinephrine.
Why did some of the No IV patients receive epinephrine, or any drug? Clearly a protocol violation. I tripped and the IV landed in the patient, is not a valid explanation.
Why did 21% of the IV group not receive epinephrine? That is not clearly explained by the authors. Were these patients resuscitated prior to initiation of an IV and administration of epinephrine?
CPR and defibrillation are indicated before drugs. Since both CPR and defibrillation have research showing that they improve the long-term outcome from cardiac arrest, it is not unreasonable to expect that cases of ROSC with only CPR and defibrillation will be the reason for some patients not receiving epinephrine.
One of the perversions of a requirement that epinephrine be given in cardiac arrest is that the 1 mg bolus dose of epinephrine, repeated every 3 to 5 minutes, is never to be given to a patient with a pulse - Never. The reason is that epinephrine is so toxic to the heart, that it could be expected to produce cardiac arrest.
There are people criticizing this study because not all of the patients in the IV group received epinephrine. They see this as a bias. Contrariwise, I see their objection as just looking for any excuse to complain about research results they do not like, even though the study's results are consistent with all of the other research that has been done. The critics fail to consider that some patients will be resuscitated prior to the point in the algorithms where drug administration is indicated. Their apparent demand that patients resuscitated prior to epinephrine administration be given epinephrine, even though the patient is no longer in cardiac arrest, is silly.
This would also not be likely to do anything to improve outcomes in the epinephrine group. The patients resuscitated prior to epinephrine administration are likely to be the patients with the briefest periods of cardiac arrest and therefore maybe the patients with the best potential for good outcomes. Returning them to a cardiac arrest, by means of epinephrine, just to follow an algorithm, would not be a good thing and it would probably have a dramatic negative effect on the survival of the patients in the epinephrine group.
The standard dose of epinephrine for a patient with a pulse, but not in cardiac arrest, is 2 mcg/minute to 10 mcg/minute. The standard dose of epinephrine for a patient without a pulse, but in cardiac arrest, is 1,000 mcg fast push every 3 to 5 minutes. I do not know of any medical professional, or any medical organization, or any medical reference, that recommends giving a living human being the dose of epinephrine that we only give to dead patients, and repeating it every 3 to 5 minutes. I would not be surprised at murder charges if the patient were to die soon after receiving this treatment that is given indiscriminately to dead patients.
Unless we can predict which patients, if any, will benefit from epinephrine, we need to find a better way to prevent giving epinephrine to the patients who will be harmed by epinephrine. If we cannot do that, we need to admit that we do not have any basis for using epinephrine in cardiac arrest.
Until there is research to show any benefit from epinephrine in cardiac arrest, we should eliminate epinephrine from all cardiac arrest treatment algorithms that are not part of well controlled studies.
^ 1 Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed - in process]
If you want to read the entire study, this link opens it in PDF.
^ 2 A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J.
JAMA. 1992 Nov 18;268(19):2667-72.
PMID: 1433686 [PubMed - indexed for MEDLINE]
BACKGROUND AND OBJECTIVE: We investigated whether the use of two different video laryngoscopes [direct-coupled interface (DCI) video laryngoscope and GlideScope] may improve laryngoscopic view and intubation success compared with the conventional direct Macintosh laryngoscope (direct laryngoscopy) in patients with a predicted difficult airway. METHODS: One hundred and twenty adult patients undergoing elective minor surgery requiring general anaesthesia and endotracheal intubation presenting with at least one predictor for a difficult airway were enrolled after Institutional Review Board approval and written informed consent was obtained. Repeated laryngoscopy was performed using direct laryngoscope, DCI laryngoscope and GlideScope in a randomized sequence before patients were intubated. RESULTS: Both video laryngoscopes showed significantly better laryngoscopic view (according to Cormack and Lehane classification as modified by Yentis and Lee = C&L) than direct laryngoscope. Laryngoscopic view C&L >or= III was measured in 30% of patients when using direct laryngoscopy, and in only 11% when using the DCI laryngoscope (P <>or= III: 1.6%) than both direct (P <>or= III) could be achieved significantly more often with the GlideScope (94.4%) than with the DCI laryngoscope (63.8%) Laryngoscopy time did not differ between instruments [median (range): direct laryngoscope, 13 (5-33) s; DCI laryngoscope, 14 (6-40) s; GlideScope, 13 (5-34) s]. In contrast, tracheal intubation needed significantly more time with both video laryngoscopes [DCI laryngoscope, 27 (17-94) s, and GlideScope, 33 (18-68) s, P less than 0.01] than with the direct laryngoscope [22.5 (12-49) s]. Intubation failed in four cases (10%) using the direct laryngoscope and in one case (2.5%) each using the DCI laryngoscope and the GlideScope. CONCLUSION: We conclude that the video laryngoscope and GlideScope in particular may be useful instruments in the management of the predicted difficult airway.
You have got to get your life together. A normal 33 year old woman does not get herself in these kinds of situations. This is the time, right now, that you need to get help. You are smoking crack, shooting up, hitching rides from truck drivers and taking random pills that they give you. You are dying. Your time is running out. I know you have probably heard this a million times, and it might not mean anything right now. I know this, but I am going to tell you anyways, because I do care, and I am sure someone out there cares too. You are only 33 years old, and you can live a whole different life, but only you can change that. Don't sit around waiting to be saved. Save yourself.
Tom B | 8:29 PM | | 3 comments
United Press International (UPI) is reporting that according to a study by the University of Michigan Health System, the chance of surviving an out-of-hospital cardiac arrest remains unchanged over the last 30 years.
The analysis of 79 studies involving 142,740 patients, published in Circulation: Cardiovascular Quality and Outcomes, found 23.8 percent of the patients survived to hospital admission and 7.6 percent lived to be discharged from the hospital.
While half of cardiac arrests were witnessed by a bystander, only 32 percent received bystander cardiopulmonary resuscitation.
"Increasing bystander CPR rates, increasing the awareness and use of devices to shock the heart and keeping paramedics on scene until they restore a person's pulse needs to occur if we are ever going to change our dismal survival rate," Dr. Comilla Sasson, the study's lead author, said in a statement.
I find this study to be interesting because it shows that only about half of cardiac arrests are witnessed. Unwitnessed cardiac arrests have a very poor prognosis, which is not surprising when you consider that this is the most time sensitive of all emergencies.
Knowing how many cardiac arrests are witnessed by a bystander is important when estimating how many "savable" cardiac arrest patients a given EMS system interacts with in a given year.
According to the best data I could find, the incidence of out-of-hospital cardiac arrest in the general population is approximately 1/10 of 1% (or 1 out of 1000).
That means that each year, a community of 50,000 people can expect about 50 out-of-hospital cardiac arrests.
If half of them are witnessed, the number is down to 25.
It's reasonable to assume that not all of those are VF/VT arrests. This isn't evidence based, but let's say that 20 of them are primary cardiac VF/VT arrests.
According to the Utstein template, the number of these patients that walk out of the hospital is a community's save rate. If the save rate is 10% then a community of 50,000 can expect 2 patients to survive to hospital discharge each year.
It's worth mentioning that most communities don't measure their outcomes at all, so this is just speculation.
Let us assume for a moment that this same community started to save 35% of its cardiac arrest patients. Instead of saving 2 patients each year they would save 7 or an additional 5.
Five may not seem like a lot of patients, but in 30 years that's 150 people, or enough to fill up a Boeing 737 (or Airbus A320).
Do you remember when Captain Sullenberger saved 150 passengers (plus the crew) on US Airways Flight 1549?
He was recognized as a hero, and justifiably so! Here's New York City Mayor Michael Bloomberg showing off the "key to the city" that was specially made for Captain Sullenberger.
Stengthening a community's "chain of survival" is a lot less dramatic than saving 150 people in a single afternoon, but we need to remember that these are real people, and they are loved just as much by their wives, husbands, daughters, son, mothers, and fathers.
So what are we waiting for?
Essential Features of Designating Out-of-Hospital Cardiac Arrest as a Reportable Event
Cardiac Arrest Registry to Enhance Survival (CARES)
As a marketing technique, many companies contact bloggers frequently to review their products. Every so often, we get free stuff in exchange for a proper review. I am an honest person, and I like to review merchandise with integrity. I also enjoy free stuff as much as the next guy. Recently I received a pair of Magnum Elite Force boots with ion-mask technology.
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I have recently had my first two articles published. They can be found at EMSresponder.com, the co website for EMS magazine. I chose a couple topics that I have spoken extensively about right here on Paramedicine 101.
Go check them out and let me know what you think. Pay no attention to the description of the ECGs in the WPW article. The wrong images were uploaded. This will be fixed shortly.
Thanks for stopping by,
Adam Thompson, EMT-P