Showing posts with label Cardiology. Show all posts
Showing posts with label Cardiology. Show all posts

Product Review: AHA's Rapid STEMI ID

Adam Thompson, EMT-P | 11:07 AM | , , | 2 comments


I was asked a few months ago to review the American Heart Association's STEMI recognition educational software.  This software was created in response to a deficit found during Mission:Lifeline.

Here is the review I gave word for word:

Link to Learn: Rapid STEMI ID

           First, I would like to say that it is not advocated to teach 12-lead ECGs in a STEMI vs. not a STEMI manor.  While the intentions seem good, there is much more to learn regarding 12-lead ECG interpretation that this type of course does not cover.  There is an overwhelming need for a more comprehensive resource for prehospital care providers, and other emergency medical personnel, for that matter. 
            It is my belief that the ACLS course should provide the base of 12-lead ECG knowledge while an online course could be adequate for continuing education.  Initial training could include the six-step method of ECG interpretation.

Six-Step Method:
  1. Rate & Rhythm
  2. Axis determination
  3. Complex, wave, and segment durations
  4. Morphology
  5. STE-Mimics
  6. Ischemia, Injury, Infarct

This method could be taught extensively while breaking down each part to include the physiology of abnormalities.  The Learn: Rapid STEMI ID course is a good start, but is at an educational level below that of what prehospital care providers should be at.  It is also not adequate enough to be part of the curriculum within a paramedic program.  I don’t feel an initial education in 12-lead ECG interpretation should be from an online course because of the inability to ask questions.
Learn: Rapid STEMI ID



Pros:
-       The interactive software is top notch.
-       The graphics used for the cardiology portion are very nice
-       For the most part the cardiology review is very factual
-       There is a good amount of ECG cases
-       The cost seems to be about right for this type of course

Cons:
-       This course is designed only for STEMI recognition, not 12-lead interpretation.  While an important part of 12-lead interpretation, it is not the only ailment that can be determined.
-       With the absence of any presentation outside of STEMI comes the lack of education regarding axis shift, rate changes, pacemaker changes, bundle branch blocks, electrolyte imbalances, etc.  It is possible to create this course in conjunction with more comprehensive resources.  For example, using the six-step method, this course would include steps five and six.
-       The cardiology review is good, but it should also be explained that some patients have slight differences in their coronary arteries (i.e. stenosis, dominant RCA, dominant Cx).
-       During the explanation of electrode application, there should be information about commonly misplaced electrodes and the need to remove all clothing on the patient from the waste up. 
-       There is no list of indications for 12-lead ECG interpretation.  While there is a good explanation of typical and atypical ACS symptoms, ACS symptoms are not the lone reason to acquire a 12-lead ECG.  Some research has shown that paramedics have not performed ECGs on nearly half of patients that present with STEMI at emergency departments. 
-       No information was provided about UA/NSTEMI, informing the learner that it is possible that the patient is suffering from an AMI in the absence of ST-Elevation.
-       It is explained how to identify ST-Elevation, Q-waves, and Hyperacute T-waves, but there is no explanation of the physiology.  A better understanding of the reasoning behind pathological changes will improve the overall efficiency of 12-lead ECG interpretation.   
-       There should be more information regarding posterior wall MI changes (i.e. reciprocal changes in septal leads, R/S ratio >1).
-       One very easy way to determine the J-point’s location is to identify the J-point in a lead above or below the lead in question.
-       Upward concavity is not a conclusive finding with early repolarization.  While the “smiley face method” is a good way to get an idea of the ST morphology, it is not the only way to differentiate early repolarization from STEMI.  Notched J-points, and mean R-wave amplitude in V2-V4 greater than 5 mm are both indicative of benign early repolarization.
-       The information on the STE-Mimics that where covered was good.  However, there is a lot more that could be provided. 
o      LVH was covered, but not RVH
o      Pericarditis symptomology is the easiest way to differentiate it from STEMI.
o      Hyperkalemia vs. Hyperactute T-waves
o      Bundle branch blocks
o      Brugada Syndrome
-       Contiguous leads should have been explained better V1 & V6 are not contiguous. 
-       The differentiation between Septal, Anterior, and Low Lateral should be made.  V1-V6 are not all considered anterior. 
-       The depth of Q-waves was not covered pathological vs. physiological.  Width was appropriately taught, but not depth.
-       It should be made known that MI is not the most common cause of ST-Elevation.

Overall, I am pleased to see that the AHA is making an attempt at 12-lead ECG education.  I am a big fan of the AHA and its use of evidence-based medicine.  In fact, there is plenty of evidence supporting ECG findings, and a need for better interpretation.  Here is an example of something that might be missed out on if this course was the base of the responding paramedic’s ECG knowledge; patient with syncope who has long QT syndrome or Brugada syndrome.  This patient may never even have a 12-lead ECG obtained even though that the two conditions described can both be lethal.  I am optimistic about the possibilities to come.  


Research: Prehospital Thrombolysis

Adam Thompson, EMT-P | 1:00 PM | , , | 0 comments

Check this out...

Also a topic within The EKG Club

Emerg Med J. 2010 Aug 3. [Epub ahead of print]
Paramedic decision making: prehospital thrombolysis and beyond.
Smith AM, Hardy PJ, Sandler DA, Cooke J.

Abstract

Background Mortality from acute myocardial infarction is influenced by the speed at which reperfusion therapy is delivered. In the UK, prehospital thrombolysis (PHT), administered by paramedics, has been developed to improve call to needle (CTN) times. Recently, it has been shown in randomised trials that mortality can be further reduced by primary percutaneous coronary intervention (PPCI). This project was developed to assess current ST-elevation myocardial infarction practice in a district general hospital and to prepare paramedics for PPCI. Methods Data were collected prospectively over a 12-month period for all patients who received thrombolysis for a presumed myocardial infarct. The primary outcome measures for each case were who delivered the thrombolysis, either the paramedic crew or the hospital, and if the patient did not receive PHT the reason why not. Secondary outcome measures included the CTN time. Results 153 patients received thrombolysis over the time period (99 men, 54 women, mean age 66+/-15 years). Of this group, 55 patients received PHT (35.9%) with a median CTN time of 36 min (inter-quartile range (IQR) 30-42 min). The commonest reason for exclusion from receiving PHT was that the patient's history did not fit the eligibility criteria (25% of cases). Conclusions Paramedics are able to deliver PHT promptly and safely. With the focus now on PPCI, it is anticipated that not only will paramedics be able to select patients for delivery to a heart attack centre for PPCI, they will be selecting many more patients for this treatment than have up to now received PHT.

So, what do you think?  Are you ready to start administering clot busters?  Here is another abstract that concludes that the early identification of STEMI improves patient outcomes.


Am J Cardiol. 2009 Apr 1;103(7):907-12. Epub 2009 Feb 7.
Effect of prehospital triage on revascularization times, left ventricular function, and survival in patients with ST-elevation myocardial infarction.
Sivagangabalan G, Ong AT, Narayan A, Sadick N, Hansen PS, Nelson GC, Flynn M, Ross DL, Boyages SC, Kovoor P.

Abstract
Shorter reperfusion times lead to better outcomes in patients with ST-elevation myocardial infarction (STEMI). We assessed the efficacy of prehospital triage with bypass of community hospitals and early activation of the cardiac catheterization team on revascularization times, left ventricular (LV) ejection fraction, and survival. Patients with STEMI (624) were divided into 3 groups determined by site of triage: ambulance field triage (163), interventional center emergency department (202), and 3 community hospital emergency departments (259). Compared with community hospital and interventional center triages, ambulance field triage resulted in a significant median decrease in door-to-balloon times of 68 and 27 minutes, respectively (p <0.001). LV ejection fraction was highest in the field triage group (52 +/- 13%) compared with the interventional center (49 +/- 12%) and community hospital (48 +/- 12%, p = 0.017) groups. Thirty-day mortality was lowest in the ambulance field group (3%) compared with the interventional facility (11%) and community hospital (4%, p = 0.007) groups. There was a significant difference in long-term survival with up to 30-month follow-up among the 3 triage groups (p = 0.041). With time-dependent Cox regression modeling the difference in survival was significant only during the first week after STEMI (p = 0.020). Every extra minute of symptom onset to reperfusion time was associated with a relative risk of long-term mortality of 1.003 (95% confidence interval 1.000 to 1.006, p = 0.027). In conclusion, field triage of patient with STEMI decreased revascularization times, which preserved LV function, and improved early survival.
And another advocating statement from 2007:

J Emerg Med. 2008 May;34(4):405-16. Epub 2007 Dec 27.
The role of fibrinolytics in the prehospital treatment of ST-elevation myocardial infarction (STEMI).
Sayah AJ, Roe MT.

Abstract
The efficacy of fibrinolytics in the treatment of ST-elevation myocardial infarction is directly related to the time of administration, with the first 2 h after symptom onset seen as a critical period for greatest improvement in cardiovascular parameters and mortality. The American College of Cardiology/American Heart Association recommends a medical contact to treatment time of 30 min for fibrinolysis in patients with ST-elevation myocardial infarction. In selected patients, reperfusion goals may be expedited with prehospital administration of fibrinolytics. In clinical trials, prehospital fibrinolysis markedly reduced the time from symptom onset to treatment, allowed earlier ST-segment resolution, and reduced short- and long-term mortality compared with in-hospital treatment. Prehospital fibrinolysis has become more feasible with the introduction of prehospital 12-lead electrocardiography, improved skills of emergency medical services personnel, improved communication with the Emergency Department, and the advent of bolus fibrinolysis. Rapid and accurate administration of a fibrinolytic is vital for the success of prehospital fibrinolysis.

Okay, that one is a bit old.  Lets open the discussion on this topic.  Let me know what you think.  Provide some better research, and I will tell you now... there is some out there.  I'd also like to hear from anyone out there that has been a part of a thrombolysis trial.

Thanks for your participation,

Adam Thompson, EMT-P

Treating Tachycardia

Adam Thompson, EMT-P | 8:15 PM | , , | 4 comments


Treating Tachycardia
By Adam Thompson, EMT-P


Tachycardia simply means a faster heart rate than normal.  With the sinoatrial node, which is the heart's inborn pacemaker, the intrinsic rate is between 60 and 100 beats per minute.  When the rate exceeds 100 beats per minute, tachycardia is present.

When treating tachycardia, it is important to first consider a compensatory cause.  The body tends to use an increased heart rate as a frequent compensatory mechanism when it senses decreased perfusion.  Two of the best dysrhythmics in the EMT and paramedic's tool box are OXYGEN and NORMAL SALINE. Both of these treatments should be attempted prior to using any other medication.  It is not advantageous to eliminate a compensatory tachycardia in a patient who needs it to perfuse.  Locating the cause of the decreased perfusion would be optimal.

Another thing to consider is the patient's hemodynamic stability.  With organized tachycardic rhythms in unstable patients, synchronized cardioversion is indicated.  There seems to be a fear amongst prehospital providers when it comes to shocking people.  The paramedic seems to be much more comfortable giving anti-arhythmic/dysrhythmic medications than they do performing cardioversion.  This is in-fact backwards thinking.  Consider Kelly Grayson's outlook on dysrhythmic drugs--they are selective cardiotoxins.  First off, they are not naturally found in the body.  Second, they metabolize over time and the reaction can be unpredictable.  Thirdly, they are used to counteract cellular depolarization.  Do you know what happens in the absence of cellular depolarization in the myocardium?  Asystole--not a common side effect, but it drives home the point doesn't it?.  Other complications, like high-grade atrioventricular blocks, and long QT syndrome may also occur.  Conversely, synchronized cardioversion doesn't have nearly as many unwanted effects.  It works fast, and goes away.  The medication you should be considering, is some sort of sedative or benzodiazapine prior to cardioversion.

Next, after determining the patient's hemodynamic stability, the width of the QRS should be considered. If the patient is stable, and they are in a sustained tachycardia, dysrhythmic medications can be considered.  It is important to determine the width of the QRS, because medications like Cardizem (diltiazem), or Adenocard (adenosine) that may be administered to narrow complex rhythms, can effectively KILL people with wide QRS rhythms.  Notice that there is not a 'ventricular tachycardia' algorithm?  It states 'Wide QRS', and lists 'uncertain rhythm' below.  This is an important concept.  If it is wide, and you are uncertain of the origin, it is ventricular tachycardia until conclusively proven otherwise.  Another reason that it is a WCT guideline and not a ventricular tachycardia guideline is because of conditions like WPW (wolff parkinson white syndrome).  With WPW, a delta wave may be present causing widening of the QRS complex.  This is important because adenosine, and Cardizem should not be administered to patients with WPW.  There is controversy regarding whether Amiodarone is safe with WPW, but as of now the American Heart Association considers it a safe option.

A wide QRS complex is considered greater than 120 ms or 0.12 seconds or 3 small boxes.


Points to remember:

  • O2 & fluids for compensatory tachycardia
  •  Synchronized cardioversion is the SAFER option
  • If QRS is wide treat as V-tach
Note: Torsades de Pointes should not be treated with Amiodarone.  This can cause lengthening of the QT interval, and subsequently a worse arrhythmia.  








Brugada Criteria.  This should only be used to confirm ventricular origin.  Not to rule it out.  

View more documents from Adam Thompson.

Videos: Acute Coronary Syndrome

Adam Thompson, EMT-P | 8:08 PM | , | 2 comments

Some stuff for you visual learners, enjoy.


This one ends abruptly, but makes a point that I like to stress, DIAPHORESIS is BAD!

Sorry for this one, but I thought it was funny






In the following video, the presenter has used some of Tom B's teaching aids to teach Sgarbossa's criteria.  I pronounce it with the 'S' by the way.  

Also check these out - video , & video

12-Lead Differential Diagnosis: Syncope

Adam Thompson, EMT-P | 2:51 PM | , , | 0 comments


12-Lead Differential Diagnosis: Syncope
By Adam Thompson, EMT-P


There are many causes of syncope. Syncope is the medical term for fainting. Most of us are pretty familiar with the common vasovagal cause. Fortunately syncope is often self-correcting; the patient hypo-perfuses, they blackout and fall, their body perfuses better, they wake up. This post will be dedicated to 12-lead presentations that may indicate causes of syncope.

I have decided to use some exerts from my favorite emergency physician/presenter, Dr. Amal Mattu.  Dr. Mattu has spoke and written on these topics multiple times.  



Bradycardia

This first one is easy, and you wouldn't even need a 12-lead to determine it's malignancy.


What do you notice about the 12-lead above? How about the rate? This is an example of bradycardia. Bradycardia may cause hypo-perfusion, leading to syncope. This would classify them as symptomatic, and they may require treatment.

*It is important to remember that there are many tachycardic arrhythmias that could cause syncope as well.   



Acute Myocardial Infarction

An acute myocardial infarction (AMI) is the most common reason we use a 12-lead for diagnostic purposes. An AMI may cause syncope amongst many other signs and symptoms.  Syncope would be an atypical (not usual) presentation for an AMI.  I am not going to elaborate much on this presentation because it requires much teaching for those who are unfamiliar with STEMIs (ST-Elevated Myocardial Infarction). Please head over to the prehospital 12-lead blog for some great education on STEMIs. 



Long QT Syndrome


Long QT Syndrome, or LQTS may lead to arrhythmias that lead to syncope.  This happens due to something called an R on T phenomenon.  The most common arrhythmia due to LQTS is Torsades de Pointes, however monomorphic ventricular tachycardia is possible.  Syncope and/or seizures are common symptoms of the rhythms associated with LQTS.

Torsades de Pointes

From Dr. Amal Mattu:


Prolonged QT-Interval  
• Prolonged QT-interval predisposes to torsades de pointes
• One of the key “can’t miss” diagnoses associated with syncope
• Perhaps a more common cause of syncope and sudden death than previously recognized?

Causes of QT-prolongation
• Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
• Sodium channel blocking medications (many!)
• Includes Type IA medications, anticholinergics, cocaine, many antipsychotics,  some antibiotics
• Acute myocardial ischemia (usually associated with inverted T-waves)
• CNS lesions, e.g. intracerebral hemorrhage (often associated with giant inverted T-waves)
• Hypothermia
• Congenital

How long is too long?
• QT-interval will vary based on patient’s heart rate
• Measure QT from beginning of the QRS complex to the end of the T-wave, and average over 3-5 beats
• “Corrected” QT-interval (Bazett formula): QTc = QT/√(RR)
• QTc is considered prolonged when > 450 msec in men and > 460 msec in women and children
• Major risk occurs in patients with QTc > 500 msec

Treatment
• Search for and correct underlying cause (e.g. correct electrolyte abnormalities, discontinue responsible medications, etc.)
• Congenital or idiopathic causes: beta-blocking medications attenuate adrenergic-mediated trigger mechanisms 
• Treatment of torsades de pointes: cardioversion/defibrillation, magnesium if relatively stable (e.g. intermittent torsades): 2 grams IV over 2-3 minutes followed by infusion
• Overdrive pacing? Isoproterenol? Atropine? These are listed as possible treatments in acquired (not for congenital) cases, but rarely needed
• Post-conversion treatment with magnesium, not lidocaine/amiodarone/ procainamide! (unlike other forms of ventricular tachycardia); for congenital cases, add beta-blocking medications


Click here or here to learn about Long QT Syndrome




Brugada Syndrome



ECG example of Brugada Syndrome


Brugada syndrome is becoming more and more well known recently.  It is associated with specific ECG changes and an increased risk for sudden cardiac arrest.  Only known cause of Sudden Unexpected Death Syndrome (SUDS)--according to Wikipedia.  The ECG changes associated with Brugada Syndrome are most visible in V1, and V2.  Non-STEMI-like ST-elevation that cannot be explained by another pathological cause (ie. LVH, LBBB, BER) may be Brugada Syndrome.  These individuals may be otherwise very healthy and/or young.

Some features of the different types of Brugada Syndrome include:


  •  a RBBB pattern in V1 without terminal S-waves in lead I and V6.  
  • A saddleback ST-elevation pattern (type 2 below)
  • Coved J-point elevation in V1, V2, V3 that gradually slopes down (type 1 below)





From Dr. Amal Mattu:

Brugada Syndrome  
More common cause of sudden death than previously recognized
• May be responsible for up to 20% of sudden deaths in individuals without structural heart disease
• Responsible for 4-5% of all sudden deaths
• Incidence varies in different populations (some genetic factors involved)
• Most common in young males (< 50 yo.)
• First onset of symptoms approximately 40 yo.
• Mortality approximately 10% per year if not treated with an internal cardioverter-defibrillator (ICD), regardless of whether or not antiarrhythmics are used  
Syndrome characterized by
• ECG abnormalities in leads V1 – V3
• Polymorphic or monomorphic (less common) ventricular tachycardia
• Causes syncope if self-terminating
• Causes sudden death if persists and not terminated by treatment
• Structurally normal heart
• Familial occurrence in approximately half of patients  
ECG findings in leads V1 – V3
• Right bundle branch block (RBBB) or incomplete RBBB pattern
• ST-segment elevation — 2 types
• “coved-type” (most common)
• “saddle-type”
• ECG findings can vary with time depending on the autonomic balance, administration of antiarrhythmic and other drugs affecting channel function, body temperature, and other unknown factors  
Definitive diagnosis can be made with electrophysiologic testing
• Challenge with an intravenous class I medication (e.g. ajmaline, procainamide, flecainide)
• Will induce increased ST-segment elevation and “coving”
• Programmed electrical stimulation of the heart
• Can induce ventricular tachycardia  
Treatment
• Placement of an ICD is the only effective treatment
• Antiarrhythmic drugs (including beta blockers, amiodarone, etc.) ineffective 

Click here or here for more on Brugada Syndrome



Hypertrophic Cardiomyopathy




From Dr. Amal Mattu:


Hypertrophic Cardiomyopathy (AKA IHSS, ASH, HOCM, etc.)

• Prevalence — 0.02% – 0.2% of the general population
• Genetic factors involved
• Hypertrophied but nondilated left ventricle
• Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall
• Cardiomegaly usually not present on chest x-ray
• Mortality 3.5% per year
• Diagnosis often made only when the patient experiences sudden death
• Usually occurs during exertion \
• Average age at diagnosis is 30 – 40 yo.
• Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion)  
ECG findings
• Normal in 7% – 15%
• Typical abnormalities
• Deep narrow Q-waves in the inferior and/or lateral leads – I, aVL, V5-6 (simulates MI, but Q-waves are “too narrow” for MI)
• Very specific for this condition
• Q-waves in lateral leads are more common than inferior leads, very commonly misdiagnosed as lateral MI
• Left atrial enlargement
• High left ventricular voltage/left ventricular hypertrophy
• Other less common abnormalities
• Tall R-wave in lead V1 (simulates posterior MI)
• Deep narrow Q-waves in the inferior leads (simulates inferior MI)
• Don’t rely on your cardiologists to make the Dx on ECG! Clinical diagnosis
• Systolic murmur at apex or LLSB
• Murmur increases with valsalva, standing
• Murmur decreases with trendelenburg position, isometric exercise, squatting
• Definitive diagnosis — doppler echocardiography  
Treatment
• Beta blockers, calcium channel blockers to improve LV filling and diastolic \function ]
• Amiodarone if ventricular dysrhythmias present 




Unrecognized Killers in Emergency Electrocardiography 
 Amal Mattu, MD 7 

PowerPoint Presentation on Strain Patterns!

Tom B | 6:23 PM | , | 0 comments

This is an awesome PowerPoint presentation from one of my favorite ECG textbooks, 12-Lead ECG - The Art of Interpretation.

You owe it to yourself to purchase this book (and no, they don't pay me to say that).

Make sure you use "full screen" so you can see all of the features of this important presentation. Pay special attention to slides 33-47!

Slide 45 shows a strain pattern from left ventricular hypertrophy (LVH).

Slide 47 shows a split screen with a strain pattern from right ventricular hypertrophy (RVH) on the left and acute infero-posterior STEMI on the right.

This is the book that taught me how to recognize strain patterns! So pay attention because this is one of the most important STEMI mimics!




See also:

Left ventricular hypertrophy - Part I

Left ventricular hypertrophy - Part II

Right ventricular hypertrophy vs. isolated posterior STEMI

62 year old male CC: Chest pain

Tom B | 4:46 PM | , , | 0 comments

62 year old male presents to the emergency department complaining of chest discomfort.


Past medical history is significant for dyslipidemia and ulcerative colitis. Also prior history of significant tobacco use. Maternal history of CAD. Maternal and paternal history of CVA.

The patient's only medication is Lipitor but he took an aspinin en route to the hospital.

Onset: Patient states the pain started that morning and became progressively worse since lunch time.
Provoke: Nothing makes the pain better or worse.
Quality: Sharp and nonpleuritic
Radiate: The pain radiates down the right arm to the bicep.
Severity: 7/10
Time: Patient states he experienced a similar pain in his right upper chest several days prior while playing tennis. He stopped exercising and the pain resolved.

The pain makes the patient feel "a little clammy." He denies shortness of breath. He states that he feels "a little dizzy" but denies palpitations. He had a negative stress test 3-4 years ago.

He has a known history of left bundle branch block.

The patient's skin is warm and dry.

Breath sounds clear bilaterally. No JVD.

Neuro exam normal.

Vital signs:

Resp: 18
Pulse: 60
BP: 140/72
SpO2: 98 on RA

A 12-lead ECG is captured and presented to the ED physician within 5 minutes of arrival.



An "old" ECG is pulled from the computer system for comparison.


What is your impression?


** Update 05/19/2010 **

After oxygen and nitroglycerin the patient reports a significant decrease in pain.

An additional 12-lead ECG is captured.


There is now slightly less ST-elevation in leads V3 and V4.

Remember that a secondary ST-segment abnormality (as opposed to a primary ST-segment abnormality) should not "improve" with oxygen and nitroglycerin!

In other words, if this ST-elevation was caused just by the LBBB, it shouldn't be "getting better". Changing ST-segments suggest the dynamic supply vs. demand characteristics of ACS!

Now, let's go back to the initial 12-lead ECG. Is the ST-elevation in the anterior leads cause for concern?

Go back and read Identifying AMI in the presence of left bundle branch block (or paced rhythm). Remember, discordant ST-elevation = or > 5 mm is the least specific of Sgarbossa's criteria! That's why we use the modified rule that I learned from Dr. Stephen Smith of Dr. Smith's ECG Blog.

That criterion states that discordant ST-elevation should not be more than 0.2 (or 20%) the depth of the S-wave in the setting of left bundle branch block (ST/S ratio).

Using that criterion, how does this ECG measure up? Let's take a look.


Ladies and gentlemen, we have a winner!

The patient was ultimately cathed and angiography revealed 100% occlusion of the LAD.

Final thought:

Does it get any more difficult that that? If Dr. Smith's decision rule works this great, shouldn't we be shouting it from the rooftops?

See also:

Discordant ST-elevation in LBBB or paced rhythm

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graph

"New" LBBB - What's the big deal?

New left bundle branch block is a poor indicator of coronary occlusion - Dr. Smith's ECG Blog

STEMI best seen in PVC (Dr. Smith's ECG Blog)

Prehospital 12-Lead ECG Efficiency

Adam Thompson, EMT-P | 10:38 PM | , , , , | 14 comments


Recently I have taken part in a very interesting discussion on the NAEMSP dialog page. This discussion is based on the paper Early Cardiac Cath Lab Activation by Paramedics for Patients with STEMI on Prehospital 12 Lead ECGs. Tom B from The Prehospital 12-Lead blog, and contributing author to Paramedicine 101 is one of the active participants in the discussion.


Some of the problems discussed:

- Poor quality ECG captures
- Deficiency in knowing when to capture a 12-lead ECG (43% of paramedics in one study did not perform a 12-lead on an active STEMI)
- Deficiency with STEMI recognition (False positives are still far to frequent)
- Poor STEMI alert and transport guidelines

One of the solutions which has a lot of supporting evidence is the transmission of 12-lead ECGs from the field to the receiving PCI facility.

Some research:

THE POSITIVE PREDICTIVE VALUE OF PARAMEDIC VERSUS EMERGENCY PHYSICIAN INTERPRETATION OF THE PREHOSPITAL 12-LEAD ELECTROCARDIOGRAM
Background. Obtaining a prehospital 12-lead ECG may improve triage and expedite care of patients with acute myocardial infarction (AMI). Whether the ECG should undergo physician review prior to activation of a percutaneous intervention (PCI) team is unclear. Objective. To document the positive predictive value (PPV) of the prehospital 12- lead ECG when interpreted by paramedics versus emergency physicians. Methods. This was a prospective, observational study. In November 2003, our local health care and emergency medical services (EMS) systems implemented a prehospital “cardiac alert” program in which patients suspected of having ST-elevation myocardial infarction (STEMI) based on the prehospital 12-lead ECG were diverted away from receiving facilities without emergent PCI capability and the PCI team was mobilized. For the first year, a cardiac alert was activated by paramedics (Phase I). After the first year, the ECG was transmitted to the ED, with the emergency physician (EP) responsible for activation (Phase II). The PPV for cardiac alerts in Phases I and II were compared by using three different “gold standards”: cardiologist interpretation of the prehospital 12-lead ECG, disposition to emergent PCI, and coronary lesions on angiography or arrest prior to emergent PCI. Results. A total of 110 patients were enrolled (54 in Phase I, 56 in Phase II). Cardiologist confirmation of a STEMI on the prehospital 12-leadEKGwas 42/54 (78%) in Phase I and 54/56 (96%) in Phase II. Disposition to emergent PCI occurred in 38/54 (70%) Phase I patients and 51/56 (91%) Phase II patients. Lesions at catheterization or arrest prior to emergent PCI were observed in 41/54 (69%) of Phase I patients and 50/56 (89%) of Phase II patients. All of these comparisons achieved statistical significance (p less than 0.01) Conclusions. Transmission to the ED for EP interpretation improves the PPV of the prehospital 12-lead ECG for triage and therapeutic decision-making.
-PREHOSPITAL EMERGENCY CARE 2007;11:399–402



Okay so a solution I would like to provide, and please provide comments here and/or on the dialog page linked to above.

My solution is to provide an adjunct course. Much like ACLS, CPR, PALS or BTLS, this course could be taught in conjunction with the paramedic curriculum but will expire and renewals would be required. The current paramedic curriculum does not include enough instruction on prehospital 12-lead ECG interpretation. My proposed course would include a whole lot more information as well as STE-Mimic recognition. Why not? In my experience, I have noticed that the biggest deficiencies that paramedics present are airway, medication administration, and cardiac rhythm interpretation--especially 12-lead ECG interpretation.

So what do you think?

Provide your thoughts or your solutions to narrowing the EMS to repurfusion times.

Congestive Heart Failure

Adam Thompson, EMT-P | 9:00 PM | , , | 3 comments

For an Anatomy & Physiology class I am taking, my professor assigned a research paper for extra credit. The topic was restrained to any of the wide variety of diseases or conditions that the human body can suffer from. I decided to chose CHF, since it happens to be something I know a little bit about. She was surprised when she asked where my references were, and I said I didn't use any. Sure, at some point, I read this information somewhere, but I couldn't remember where if I tried. Guess I skipped the research part of this research paper. Anyhow, I figured I would share it. I have posted on CHF before and covered most of this, but a refresher never hurt anyone and this is much more basic.



Congestive Heart Failure

Congestive heart failure, or CHF, is a condition that afflicts millions of Americans. Over five hundred thousand new diagnoses are made every year. CHF is a condition that is entirely caused by the body’s homeostatic compensatory mechanisms. CHF arises from the condition simply termed, heart failure.

Heart failure is manifested by the heart’s inability to provide adequate perfusion to the body. This occurs due to other conditions or diseases such as chronic hypertension or a previous myocardial infarction. Clinical findings may include a decreased blood pressure, dizziness, or signs of hypoxia.

The body senses this decrease in cardiac output and attempts to maintain homeostasis. Baroreceptors detect inadequate pressure and norepinephrine is released by the adrenal gland. This causes profound vasoconstricion, as well as an increase in inotropy, chronotropy, and dromotropy. This just means that the heart is beating faster and harder due to the catecholamine release. The kidneys also lend a hand by releasing Angiotensin Converting Enzyme, or ACE. ACE converts angiotensin I into angiotensin II, which is yet another vasoconstrictor. The body will also act to increase volume by inhibiting fluid release. The heart itself produces a peptide called Brain or B-type Natriuretic Peptide (BNP).

All of these compensatory mechanisms acting together cause the cardiovascular system to go into overdrive. Too much vasoconstriction and cardiac force cause increased afterload. Afterload is the pressure in which the heart is pumping against. This is also known as arterial pressure and an increase results in an increase in palpable blood pressure. Since the heart can’t pump blood out efficiently against the increased after load, blood backs up. It first backs into the atria from the left ventricle. It then backs up into the pulmonary vein and then the lungs. This is where we get the congestion of congestive heart failure.

Pulmonary congestion is also known as pulmonary edema, and may be a lethal condition. Chest X-rays and BNP levels are used to diagnose CHF patients. Due to the increase in workload, the myocardium of the heart hypertrophies and shows up as an enlarged heart on a chest X-ray. Chronic CHF patients are treated with oral diuretics, and antihypertensives such as beta blockers and ACE inhibitors. The beta-blockers decrease the rate of contraction and ACE inhibitors block the Angiotensin Converting Enzyme.

Emergency treatment may include bronchodilators, nitrates to decrease preload and afterload, and continuous positive airway pressure, also known as CPAP. CPAP provides a continuous flow of air that keeps the alveoli open while forcing the fluid back out of the lungs via pulmonary capillaries, and back into the cardiovascular system. Nitates and CPAP have shown to drastically improve the outcome of emergency CHF patients with marked hypoxia.

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