Hi Darlene,
I am a nursing student at Western University and had the privilege of participating in this course this calendar year. I have been watching it bit by bit in between my studies (I am a CTF student so classes are intense and year round).
I have finally completed the course just now. I loved it. It was well done and I hope to refer to it many times over my career. It in fact helped me understand some cardiac conditions and strip characteristics better than how it was explained to me in my program to be quite honest.
Kindest Regards,
Nadia
For those of you who have never seen how adenosine works, this is a great example of why patients report feeling horrible when given it.
This case wonderfully demonstrates a narrow complex tachycardia and how the administration of adenosine may not always revert the tachycardia to sinus rhythm.
http://hqmeded-ecg.blogspot.ca/2017/08/what-happens-when-you-give-adenosine-to.html
Our 2023 OnDemand courses are now being offered with the option to complete as a Certification Course. Contact us for more information or visit our Courses page - OnDemand for further detail.
The QRS complex reflects ventricular depolarization and by most standards, should be no greater than 0.12 seconds. When the QRS complex is wider than 0.12 seconds the ST segment automatically becomes altered in the opposite direction to the QRS complex. This normal opposing ST-to-QRS complex phenomenon is known as ST discordance. There are various reasons why a QRS will widen and when it does, it signifies that the time it takes for ventricular depolarization to occur is taking longer than normal.
A bundle branch block is the most common cause of a wide QRS complex; however, other causes include a pacemaker rhythm, a ventricular rhythm and the use of an accessory pathway such as Wolff Parkinson White. Hyperkalemia may cause a ventricular rhythm. Whenever a new wide QRS complex is seen we need to be concerned about “WHY”. One of the most common causes of a sudden widened QRS complex, such as a bundle branch block, is an Acute Coronary Syndrome or Coronary Artery Disease. In our assessments of the causality, we will conduct a cardiac workup consisting of an ECG, Echo, and some form of Stress Test. Depending on these findings, the person may then require diagnostic cardiac catheterization to determine appropriate therapy: medical vs interventional management.
The biggest problem with a wide QRS complex and the ST discordance is that the ECG is often rendered non- diagnostic in determining if an ACS is present. Some call this phenomenon of ST discordance a STEMI Mimicker, meaning the ECG will look as if the patient is having a STEMI when they are not. The concern in a STEMI Mimicker is that the patient will be inappropriately treated as a STEMI which may lead to harm. Others call this phenomenon of ST discordance a STEMI Masker, meaning the patient will not be diagnosed and treated as a STEMI because the ECG was non-diagnostic. Mortality and morbidity are higher if we do not provide reperfusion therapy to a STEMI.
I’m of the camp that feel an ECG with a LBBB should be considered and treated like a STEMI until proven otherwise, especially if the patient is having cardiac symptoms. Err on the side of caution that time is muscle. As a CCU nurse in the pre-fibrinolytic and PCI era, patients who presented with chest pain and a LBBB had very high mortality. Then came the numerous GUSTO and ASSENT studies looking at Streptokinase, t-PA, r-PA, TNK and we were given an amazing drug intervention that could dissolve the clot in a STEMI resulting in reduced mortality.
In those days, the patient who was experiencing classic symptoms of a MI but who also had a LBBB would not be giving fibrinolytic therapy because the risk of harm in getting this drug was thought to be too high given we weren’t 100% sure of a STEMI on the ECG. As it turned out, research showed that the mortality was greater in not treating these patients and it was discovered, with the advent of cath labs, that these patients who presented with symptoms and a LBBB were often experiencing an occlusion in the proximal left anterior descending artery causing a massive anterior or anterolateral MI.
Given this new data, the guidelines for inclusion of fibrinolytic therapy were then revised so that a patient with symptoms of a STEMI plus a presumed new LBBB could be given fibrinolytic therapy as long as there were no contraindications. The harm in not giving an anterior or anterolateral STEMI intervention is that they will end up with any of the following: severe left ventricular dysfunction (Grade IV LV; a.k.a. HFrLV), left ventricular remodelling leading to a high rate of cardiac arrest, ventricular rupture, NYHA Class III symptoms (inability to do most of their activities of daily living without having symptoms, a.k.a“cardiac cripple”), and high burden of cost on the health care system
Then new research came out indicating that we sent too many patients to the cath lab who were having symptoms plus a LBBB and many of these patients were actually not having a STEMI. The inherent risks of going to the cath lab caused a shift, yet again, in practice guidelines. Instead of erring on the side of caution in treating the symptomatic LBBB like a STEMI until proven otherwise, the shift trended to erring on the side of caution and treating the LBBB as a STEMI mimicker. I predict that research will show this less-aggressive management will result in high mortality... time and research will tell.
For those of you who believe more that a LBBB should be treated like a STEMI Mimicker I would strongly suggest you become very familiar with Dr. Sgarbossa and Dr. Cai’s work on diagnostic criteria of a STEMI on an ECG with a LBBB. There are numerous case studies that have demonstrated the positive predictive value of this assessment tool and I believe strongly that we should all incorporate this tool in assessing the ECG with a LBBB in a patient presenting with symptoms. Also consider the diabetic who is presenting with vague symptoms and a LBBB. If this is a known new LBBB, we need to ask ourselves why they have suddenly developed it.
In my opinion, an ECG with a LBBB should be considered neither sensitive (diagnostic for a MI: masker) nor specific (not diagnostic for a MI: mimicker). The assessment for Sgarbossa criteria needs to be examined further and applied to all ECG with LBBB. However, as Dr. Sgarbossa said herself, the absence of meeting her criteria in a LBBB does not rule out the presence of a MI. Bottom line: the management of a patient with symptoms of a STEMI and a LBBB needs to considered high priority and the age old saying “time is muscle” needs to be kept in the forefront of our approach to treatment.
Please let me know if you liked this article by sending me an email or just forwarding it to your friends/colleagues on social media.
References:
Cai, Q., Mehta, N., Sgarbossa, E. 2013. Am Heart J
Sgarbossa E., et al. 1993 N Eng J Med
Smith,S., et al. 2012. Annals of Emerg Medicine
This month’s blog is about a topic that has been of immense interest to me my entire career: the QT Interval. My first exposure to the QT interval was as a CCU bedside nurse, and our practice at that time was to assess the QT interval on all patients that were started on anti-arrhythmic medication. Then, as a research nurse in Cardiovascular and Diabetic clinical trials, I noticed a shift in the FDA and Health Canada when they made it mandatory in their Phase II and III Clinical Trials to measure the QT interval before starting on the study medication and periodically throughout the clinical trial. The importance of QT interval measurement became more apparent to these federal agencies because of all the known drug-to-drug interactions and, more importantly, because of the unknown drug-to-drug interactions.
For over 20 years, I have been asking participants at the Rhythm and ECG courses that I teach how often they measure the QT interval and in which patients. In 2008, my initial research on the practice of routine QT interval measurement was published in the Canadian Association of Critical Care Nursing, and my findings were that of 180 nurses working with patients on cardiac monitors/telemetry, only 30% of nurses reported that they always measure the QT interval when performing their rhythm assessment. More impressively, 45% reported they only sometimes measure this interval and 25% reported they never measure this interval.
So, ten years after this research was published, has practice changed? I would hope so. Given FDA and Health Canada’s increased awareness, increased knowledge of drug-to-drug interactions, and technology where electronic medical records are available among health care interdisciplinary teams allowing for a more-thorough assessment of the patient’s polypharmacy regime, one would feel safe to assume that the routine measurement of the QT interval was common practice to all who assess rhythms and ECGs. However, I am still polling my participants and still frequently seeing less than 40% acknowledge that they look at the QT interval with every patient and every rhythm strip analysis. I believe a practice gap continues to exist and I would really like to re-evaluate this issue again and address areas where we can focus on improving this gap.
I have many questions: how many nurses in critical care routinely measure QT interval? How many nurses in the Emergency Department routinely measure this interval? What about the nurses working on Telemetry? And, lastly, what about staff working with the patient who is pre-hospital or in out-patient clinics? How have guidelines and recommendations changed over the past ten years and what are the current guidelines?
Starting in April, I will be incorporating an assessment tool in my ECG and Rhythm workshops that will ask those meeting certain criteria, to answer a series of questions addressing their practice of rhythm interpretation specific to the QT interval. I am looking forward to readdressing this topic and getting some facts on what is really happening out there. I’ll keep you posted on my findings.
Great question asked by Stacey, who is the nurse educator in a northern rural hospital. As many of our readers, like Stacey, are hours to their closest PCI center, their STEMI protocol is to administer TNKase upon meeting the criteria checklist.
The question I was asked is: "why is the Cardiac Care Network recommending NOT starting the IV in the right wrist or hand?"
I checked the Cardiac Care Network's(CCN) website and found the following two documents for reference:
RECOMMENDATIONS FOR BEST-PRACTICE STEMI CARE IN ONTARIO
ACS MANAGEMENT RECOMMENDATIONS FOR REMOTE COMMUNITIES
I was not able to find a direct CCN policy statement or a TNKase manufacturer’s statement indicating which hand to start the IV in. However, the CCN document did provide examples of various organizations' documentation for CODE STEMI in outlying regions. The example from Thunder Bay Regional Health Centre did indicate to start 2 IVs and to avoid right wrist or hand.
Wanting to know the rationale for this policy, I asked my QRS colleagues who work in the cath-lab or in an organization where PCI is standard practice for their STEMI patients. Their responses were all identical: if the patient requires rescue PCI they generally use the right radial artery. They use the right radial because the left is a really tight angle and very challenging to access the coronary ostia. Another response from one of QRS instructors is, would you even want to put a peripheral IV in the hand or wrist of a STEMI patient who is in any way unstable or has the potential to become unstable? Putting IVs in joint areas is usually problematic because patients move their hands and wrists. You always want to ensure readily available venous access for emergent medication or volume administration should the patient deteriorate.
Thanks to Catherine, Betty Anne, Sevi, and Suzanne for their input. Thanks to Stacey for the question.
References:
http://ccn.on.ca/ccn_public/uploadfiles/files/ACS_management_in_remote_communities_FINAL_Sept_2013.pdf
http://www.ccn.on.ca/ccn_public/uploadfiles/files/Recommendations_for_Best_Practice_STEMI_Management_in_Ontario_(6).pdf
Peri-arrest is defined as the moments just prior to and after a cardiac arrest. With good assessment skills and prompt intervention, peri-arrest situations may be avoided. Many in-hospital arrests are preceded by recognizable physiologic changes, many of which are evident with routine monitoring of vital signs. In recent studies, nearly 80% of hospitalized patients with cardiorespiratory arrest have abnormal vital signs documented for up to 8 hours before the actual arrest (Heart and Stroke Foundation, 2017). Untreated early shock and respiratory distress lead to cardiovascular collapse.
The New Heart and Stroke Foundation ACLS for Experienced Providers is now available through QRS.
Answer this short questionnaire to find out if you would benefit from this course:
- Are you looking to strengthen your clinical skills?
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- Have you done ACLS more than once?
- Are you planning to do an ACLS recertification in 2018?
If you answered “YES” to all these questions, please consider your next ACLS course an ACLS Experienced Provider course. Through focused, interactive case discussions, the 1-day ACLS EP course goes beyond the algorithms to gain better knowledge of the processes involved in the patient’s condition. The opportunity to finely tune your assessment skills will lead to improved patient outcomes.
Check out the spring ACLS EP COURSES poster on our FACEBOOK page or website courses and reserve your spot today!
Before starting this month’s case study, I would like to ask our readers two questions to get the gray matter going. These are standard questions I ask when running my courses:
What is the normal “pacemaker” of the heart? What rate does it normally fire at?
How would you be able to differentiate a supraventricular beat vs a ventricular beat?
The answers will be viewed at the bottom of this case.
With those questions asked, let’s move on to the case study which was presented in Dawn Altman’s site, ECG Guru. Thank you Dawn, it’s always a pleasure to feature your cases.
Case: A 60-year-old male is brought into the Emergency Department by EMS. He was involved in a MVC, sustained no apparent injuries but is severely intoxicated. He is hemodynamically stable with a heart rate of 170/minute.
Below is the first ECG taken at 1507hrs. What do you think this rhythm is?
a. SVT b. Sinus Tachycardia c. Atrial Flutter d. VT
Rate: 170/min and regular. Intervals: P wave – even though the rate is rapid, there is evidence of a P wave prior to each QRS complex. The PR interval is the same. QRS – narrow. Rhythm: Sinus tachycardia. Discussion: The release of stress hormones combined with his intoxication put this patient into a sinus tachycardia. Many may think that any narrow complex tachycardia over 150/min is SVT. SVT can be an atrial flutter, atrial tachycardia, re-entry tachycardia. Oftentimes, we label a narrow complex tachycardia SVT because we are unable to distinguish identifiable features to specifically label the rhythm: such as P waves or flutter waves. In this ECG, there is evidence of one P wave prior to each QRS complex, making this tachycardia likely sinus in origin.
Below is the second ECG taken at 1543hrs. What is the rhythm?
Note that all complexes are still the same; however, the rate is now 110/min. The rate has gradually decreased from the initial ECG, which supports sinus tachycardia vs. the other SVT options that were discussed.
Conclusion: a narrow complex regular tachycardia less than 150/minute is sinus tachycardia. A narrow complex regular tachycardia over 150/minute may still be sinus tachycardia and may be challenging for the health care provider to properly interpret. Is it SVT or is it Sinus Tachycardia? This is a very important question to answer properly because treatment varies greatly between the two. When deciding SVT vs Sinus Tachycardia, look at the story and presentation. And, here is a great tip: A gradual increase or gradual decrease in the rate occurs in a sinus tachycardia. Whereas for SVT, the rates suddenly increases or suddenly terminates.
Thanks again to Dawn for this great reminder.
Answers to the 2 questions above:
1. The Sinus Node is the normal pacemaker of the heart and usually fires between 60-100/minute. The hallmark of a sinus rhythm is a P wave prior to each QRS complex. Sinus rhythm can be faster than 100/minute = sinus tachycardia or slower than 60/minte = sinus bradycardia. 2. Supraventricular tachycardia originates above the ventricles; therefore, the QRS duration should be normal (unless there is also a bundle branch block). Ventricular tachycardia is always a widecomplex regular rhythm.
This was a randomized clinical trial looking at utilizing a modified Valsalva technique to convert supra ventricular tachycardia (SVT) to sinus rhythm. The results of applying the modified Valsalva technique demonstrated a 43% conversion rate versus a 17% conversion rate with standard Valsalva technique.
The best way to describe this modified technique is for you to watch this short (2 minutes) You tube video presented by one of the investigators of the REVERT study. This is a great technique that all emergency personnel should be thinking about implementing next time faced with a patient in SVT.
Modified Valsalva – REVERT Study - https://www.youtube.com/watch?v=8DIRiOA_OsA
