Stemi

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Comment by ZOLL RescueNet on October 15, 2009 at 3:50pm

Looking for a little cardiology education? The American Heart Association has online courses. Titles include:
HeartCode™ ACLS part 1
Learn:™ Rapid STEMI ID
HeartCode™ PALS
....and many others. Check it out.

http://www.onlineaha.org/index.cfm?fuseaction=info.acls

Comment by Rob Theriault on September 20, 2009 at 7:32am

I recently developed a series of over 30 mini enhanced Podcasts covering 12 Lead ECG interpretation and including STEMI review. You can find them on my blog: Paramedic Tutor under the eLearner tab.

Comment by Stephen Irons on September 8, 2009 at 8:23am

Hi All,
I'm the Advanced Care Clinical instructor for the ambulance service of New South Wales Australia. We have two programs running at the moment. 1st is the early triage of acute myocardial infarction ETAMI. This is a metropolitan based ED bypass to the cath lab for PCI. I started this project in collaboration with 2 major PCI centers in 2004 and it has been extremely successful. We are published in the European Heart Journal and I am one of the co authors. To date we have provided 850 STEMI's successfully for rapid reperfusion which is not too bad for only 2 hospital catchment areas.
Our second program is the prehospital thrombolysis proof of concept for a particular rural demographic. This has been running for approx 15 months. The drugs of choice include Metalyse followed by Clexane. We have identified 24 STEMI's and have reperfused 14 as we have a strict inclusion exclusion criterion. some of the other STEMI patients received accelerated thrombolysis at hospital as quickly as 4 minutes after we hit the door. Of course some did not.

Cheers from Australia
Stephen

Comment by ArcticKat on September 7, 2009 at 12:48pm

Sorry, I'm not in he United States, otherwise I'd provide you with our BLS 12 Lead protocol.

Comment by Jon P. Cloutier on September 7, 2009 at 11:24am

Historically, the use of 12-lead ECG has been a function of ALS but times are changing. In EMS today, 12-lead ECG interpretation remains largely a Paramedic skill however, the simple act of acquiring and transmitting a 12-lead ECGs does not require an ALS skill set.

I am interested to know where in the United States, a BLS provider (First Reponder, an EMT-Basic, an EMT-Intermediate in BLS environment) is permitted by Scope of Practice to acquire and transmit 12-lead ECGs.

Comment by Sam Dabaja on April 14, 2009 at 8:39pm

Please view and comment.
Sam

Comment by ArcticKat on April 14, 2009 at 3:02pm

Myoglobin, creatine kinase, and troponin I are proteins found in cardiac muscle cells and are released into the blood upon damage or death of cardiac tissue.

Myoglobin is an oxygen-binding heme protein with a molecular weight of 17,800 daltons, normally found in skeletal as well as cardiac tissue. It constitutes about 2% of the total muscle protein and is located in the cytoplasm of the cell. Also found in the cytoplasm is creatine kinase (ATP: creatine N-phosphotransferase, (CK). CK catalyzes the reversible phosphorylation reaction of creatine with ATP.

In humans, isoenzymes of CK have been identified in both the cytosol and mitochondria of cells from a wide variety of tissues. Cytosolic CK exists as a dimeric molecule formed from two types of single-polypeptide subunits, designated “M” and “B”. Each subunit has a molecular weight of approximately 41,000 daltons and distinct immunologic epitopes. These two subunits combine to form three different isoenzymes of CK: CK-MM, CK-BB, CK-MB. The relative abundance of the particular isoenzyme is dependent on the tissue being examined. The CK-MM isoenzyme is predominant in skeletal muscle tissue, while the CK-MB isoenzyme is most abundant in cardiac muscle tissue. Troponin I (TnI) is part of the troponin complex which, together with tropomyosin, forms the main component that regulates the Ca++-sensitive ATP-ase activity of actomyosin in striated muscle (skeletal and cardiac). The troponin
complex consists of three subunits, troponin T(TnT), troponin I(TnI), and troponin C (TnC). Each subunit has a distinct function with TnC as the site of Ca++ binding, TnT the tropomyosin binding, and TnI as the inhibitory subunit. Different isoforms of TnI exist in the skeletal and cardiac muscles (sTnI and cTnI, respectively) with distinct immunologic epitopes that allow the production of cardiac-specific TnI antibodies.

The cardiac markers myoglobin, CK-MB, and troponin I have been established as useful tools in the diagnosis of acute myocardial infarction (AMI). Since the temporal release patterns of the three markers have significant differences, all three are useful tools in the determination of the source and timing of the onset of chest pain. Cell injury from AMI has been shown to result in a level of blood myoglobin above the upper limit of normal in approximately 2-3 hours after the onset of chest pain. Maximum concentrations are generally observed after 9-12 hours. CK-MB and troponin I are found in blood at elevated concentrations approximately 4- 6 hours after the onset of chest pain and peak at 12-24 hours. However, whereas CK-MB levels return to normal values in about 72 hours, troponin I levels remain elevated for up to 5-7 days. The use of these three markers is therefore complementary since they detect cardiac tissue damage over a wide range of times after myocardial infarction.

Myoglobin/CK-MB/Troponin I Tests employ a solid-phase chromatographic immunoassay technology to qualitatively detect the
elevation of myoglobin, CK-MB, and troponin I in human blood samples. When a sample of blood is dispensed into the sample well, red blood cells are removed by the separation filter and the plasma migrates into the test membrane. Myoglobin, CK-MB and troponin I present in the sample bind to specific antibody-dye conjugates and migrate through the Test area containing immobilized anti-CK-MB, anti-myoglobin, and streptavidin. The cardiac marker-antibody-dye complexes bind to the corresponding immobilized antibodies or streptavidin in the Test area. Unbound dye complexes migrate out of the Test area and are later captured in the Control area. Visible pinkish-purple bands will appear in the Test and Control areas if the concentrations of one or more of cardiac markers, myoglobin, CK-MB, or troponin I, are above established cutoff values. If the CK-MB concentration in the specimen is 5 ng/mL or greater, a band is present in the CK-MB area. If the myoglobin concentration in the specimen is 50 ng/mL or greater, a band is present in the myoglobin area. If the troponin I concentration in the specimen
is 1.5 ng/mL or greater, a band is present in the troponin I area. If a band is present only in the Control (C) area, the test result is read as negative, indicating that the myoglobin, CK-MB, and Troponin I concentrations are all below the cutoff values. If no band is present in the Control (C) area, the test is invalid and another test must be run, regardless of the presence or absence of band(s) in the Test Area.

Copied from www.tntdiagnostics.com information pamphlet

We've been using these devices for about a year now and I can't say anything but good things about them. They've even been instrumental in diagnosing a few NSTEMIs.

Comment by Jim on April 14, 2009 at 2:30pm

Reverse Cardiac Arrest
Andrew Muck, Micheal Hilliard, MD, Bruce D. Adams, MD
March JEMS bonus
2009 Mar 4
Just because cardiac arrest survival rates have stagnated over the past 30 years doesn't mean providers should be pessimistic about every call for pulseless electrical activity (PEA). There are several cases in which cardiac arrest can have positive outcomes, including hypothermic cardiac arrest, cold-water drowning and toxicologic cardiac arrest.

As we consider the specific clinical scenarios in which cardiac arrest can have good outcomes despite prolonged CPR, let's review some reversible causes of cardiac arrest that can also have positive outcomes. Reviewing the classic "Hs and Ts" of PEA arrest offers a concise way to review some other reversible causes of cardiac arrest in a practical manner that can be remembered and applied in the prehospital setting. (1,2)

The Hs and Ts of Pulseless Electrical Activity
Cause Treatment
Hyothermia Warming, both active and passive
Hypoxia Airway and oxygenation
H+ (acidosis) Improve with overall resuscitation, sodium bicarbonate
Hyperkalemia Albuterol, insulin with dextrose
Hypovolemia Stop any bleeding, fluids, blood products
Thromboemboli Resuscitation, consider thrombolytics
(lung-pulmonary embolism)
Thromboemboli Resuscitation, consider thrombolytics
(heart attack/myocardial infarction)
Tamponade (periocardial) Periocardiocentesis
Tension pneumothorax Needle thoracostomy
Toxins Charcoal

References

Benson P, Eckstein M: "Pulseless electrical activity: A Case Conference." Prehospital Emergency Care. 9(2):231–235, 2005.
Koeck WG: "A practical approach to the aetiology of pulseless electrical activity. A simple 10-step training mnemonic." Resuscitation. 30(2):157–9, 1995.
Capt. Andrew E. Muck is the assistant director of EMS at Wilford Hall Medical Center at Lackland Air Force Base in Texas. He has served in the United States Air Force for five years and much of this article was written while deployed in Iraq. His recent work has included coordinating a hypothermia protocol for cardiac arrest at his institution. Contact him at Andrew.Muck@lackland.af.mil.

LTC Michael Hilliard is the transitional year program director and staff emergency medicine physician at the San Antonio Uniform Health Education Consortium at Brooke Army Medical Center. He has enjoyed a wide variety of assignments in his career, including time in Baghdad, Iraq, and is currently assigned to the teaching center in San Antonio, Texas.

COL Brice Adams is the chief of emergency medicine and also chief of clinical research at William Beaumont Army Medical Center in Texas. He has enjoyed a wide variety of assignments in his career, ranging from combat assignments to teaching centers. His research and teaching interests focus on resuscitation, trauma and combat casualty care.

Read “When Dead is Only Mostly Dead.”


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Comment by Jim on April 14, 2009 at 2:17pm

Find more videos like this on JEMS Connect - EMS Emergency Medical Services

Comment by Jim on April 14, 2009 at 2:08pm

Prehospital 12 lead ECG programsPosted by Tom Bouthillet on December 10, 2008 at 8:02am in ALS Issues and Ideas
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Does your service perform prehospital 12 lead ECGs?

Does the prehospital 12 lead ECG help determine your transport destination?

Is the cath lab activated based on the prehospital 12 lead ECG?

Does your program rely on the paramedic interpretation of the 12 lead ECG? Does your program rely on computerized interpretation of the 12 lead ECG? Does your program rely on off-site interpretation of the 12 lead ECG by a physician? Does your program utilize a combination of these three methods?

If the prehospital 12 lead ECG is transmitted for off-site interpretation by a physician, what technology are you using? What is the failure rate? How is the data quality?

What was your initial education in 12 lead ECG interpretation?

Did it include a strong emphasis on STE-mimics (left bundle branch block, paced rhythm, left ventricular hypertrophy, benign early repolarization, pericarditis, hyperkalemia, etc.)?

Is there anything notable about your QA/QI process (regular multidisciplinary meetings at the hospital, data sharing, every 12 lead ECG reviewed by the Medical Control Physician, paramedics taken out of service and allowed to watch the cath procedure, etc.)?

Is your state involved in regionalizing STEMI care (similiar to trauma)?

How often are you called to the local community hospital for interhospital transfer of STEMI patients for primary PCI?

What has been the biggest barrier to the success of your prehospital 12 lead ECG program?

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