T wave Abnormality

ACLS : some point not to forget

Pr; < 0.12 Sec

QRS: ,0.12 sec

QT<0.460sec

VF:

FIne vs COarse VF, 

Not VF or pulseless VT

PEA: 

electromechanical Dissociation

narrow complex usually caused by condition iutside the heart but Wide complex usually caused by heart

Not VF or pulseless VT

ASystole:

Pwave might me present but no R wave/ ventricular activity

AFT: 

atial rate 220-350

FLutter wave usually occupieause s 1 big box

AF: 

Atrial rate 300-400

Reenterant SVT: 

220-250 rate usually

P waves are not usallly seen  cause fuses with T wave cause of rapid heart arte

So looks like Sinus tachy but rhythm is fast

Ventricular tachyarrythmia:( check for QT prolonging drugs)( Anti muscaranic)

VT> 30 sec----sustained VT, 

<30 sec duration is Unsustained VT---dont req intervention

3 consecutive PVC: means VT

ventricular rate > 120-250

 p wave present but not seen < AV disscoiation>

Torsa de:

QT prolongation--------increase RRP---so increase risk of arrythmia

* difficult to distinguish type 2b AV block from AF

Pediatric Defib dose is 2-4 J/kg

 bBrady:

if symptomatic----- then gv ATropine 0.5mg I V bolus q 3-4 min---------if no response gv TCP or meds like dopa or epi at a rate of 2-10mcg /min-----------id still no response to TCP the  consider TVP

• During CPR : coronary perfusion pressure > 10mmhg--------------but this cant  be done during cpr so Intra arterial relaxation pressure < 20 mmhg 

end tidal co2--< 10 indicates inadequate CPR..

• Chest recoil ------increase increase coronary perfursion pressure
• 100 heart rate improves ROS and Neurological outcome...( proved)
• for uncoscious pt: tidal volume requirement is around > 500-600ml
• half a bag squeeze is adequate to fill the lungs and chest rise
• Excessive ventilation: cause gastric inflation, decrease venous return and decrease survival

ACLS:

• imp to give complete 2 min of CPR
• Amidarone  for refractory VF/VT
• Epinephrie to all card arrrest pt eveyry 3 -5 min
• Atropine No longer used for PEA and pulseless electrivity or Asystole.

Perfusing rythm:

•  regular monomorphic Wide complex Tachy: If source of Tachy is not known then use Adenosine
• If regular  mono narrow complex tachy---use adenosine
• But for irreg wide complex tachy: dont use adenosine ow cause degn of rythm to VT
• Brady cardia:  Atropine for all brady------if ineffective then use either chronotropic agent like epi or dopa= tc pacer

Suchronised Cardioversion:

•  for unstabel Atrial Fibrillation: dose 120-200 j ( biphasic)
• for unstable AFT or SVT: 50-100 j

for monophasic waveform:

Initial dose 200 j then increase in step wise manner

FOR UNstable VT: initial dose is 100j ---if no response increase the dose

post Cardiac arrest carre:

• Therapeutic Hypothermia is the only intervation shown to improve neurologic recovery: gives esp in coatose pt after ROS and VF as a [resenting rhtythm: cool down body to 32- 34'c for 12-24 hrs
• STMI pt hypothermia and PCI

AIRWAY Management:

• CApnography: most reliable indiactor of ETT and eff of chest compression
• Endtidal co2 normally is 40mmhg...if ineffective chest compression then blood flow to lung decrease and co2 diffusion also decrease ---decreasing endtial c02

 Goals of reperfusion treatment:

•  PCI within 90 min of arrival to ED
• fibrinolytic t/t within 30 min of arrival to ED

 STroke:

pt should recive fibrinolytic t/t within 3 hrs of onset of symp or for slelcted pt windows has been increase to 3-4 and half hrs...( bt not approved by FDA yet)

LVH/ repolarization defects vs STEMI

One of the most confusing ST-elevation mimics is the “strain pattern” (or repolarization abnormality) occasionally found with left ventricular hypertrophy.
This is important because left ventricular hypertrophy is one of the most common causes of ST segment elevation in chest pain patients.
Many 12 lead ECG classes teach to recognize the voltage criteria for LVH (or at least one of the voltage criteria) but I don’t think most 12 lead ECG classes do an adequate job explaining exactly what a “strain pattern” looks like.
As a result, once the student identifies the voltage criteria for LVH, the interpretation stops. Similarly, once the student identifies the presence of “wide” QRS complexes, the interpretation often stops.
It’s as if we’re teaching students that it’s impossible to identify STEMI in the presence of baseline abnormalities.
It’s more difficult, but it’s certainly not impossible. The whole point is to know what a “normal” abnormality looks like. This is not an oxymoron! It’s the key to advanced 12 lead ECG interpretation.
In many cases, an ECG can meet the voltage criteria for LVH but show only minimal distortion of the ST segments and T waves. In other cases, the ECG will show the characteristic ST segment depression and T wave inversion in the lateral leads, but not the exaggerated ST segment elevation and T wave prominence in the right precordial leads.
Let’s look at some examples. Let us assume that we are dealing with a patient complaining of chest discomfort.

ECG courtesy of Dr. Jonas de Jong and ECGpedia.org

This is exactly the kind of ECG that gives  a lot of trouble. It demonstrates a strain pattern (or repolarization abnormality) with left ventricular hypertrophy. The good news is that it’s a very typical looking strain pattern!
Since this 12 lead ECG is not in the standard U.S. format, I used “cut” and “paste” to structure it into a pattern more typical of prehospital 12 lead ECGs in the U.S.

In the first place, you will notice that the rhythm is sinus at about 75 beats per minute (using the large block method).

The frontal plane axis is probably around 30 degrees (40 degrees if you correct by 10 degrees due to the fact that lead III is slightly positive). This is important because a common misconception is that left axis deviation will be present with left ventricular hypertrophy. By no means is this always the case!
The QRS width is less than 120 ms, so we know that we’re not dealing with a bundle branch block.
What about the ST segment elevation and huge T waves in the right precordial leads! Surely this patient is experiencing acute anterior STEMI!
Negative, ghostrider! (For my international friends, this is a reference to the movie Top Gun).
Let’s look at the relationship between the QRS complex and the T waves in this ECG. The general pattern is one of discordance. In other words, When the QRS complex is positive (especially in the lateral leads I, aVL, V5 and V6) the T wave is negative. This is sometimes referred to as a widened QRS/T angle.
In addition, the ST segments are downwardly concave and the T waves are asymmetrical.
These are the cardinal findings with strain patterns (or repolarization abnormalities) secondary to left ventricular hypertrophy.
This ECG also shows ST segment elevation in the right precordial leads (V1, V2 and V3). You will note that the ST segments are upwardly concave and the severity of the ST segment elevation and T wave height is proportional to the depth of the S wave.
This is extremely important! With left ventricular hypertrophy, the deeper the QRS complex, the higher the ST segment and more pronounced the T wave abnormality.
This is also true of the ST segment depression and T wave inversion typically found in the lateral leads. The higher the R wave, the deeper the ST segment depression and more pronounced the inverted T wave.
Consider the following graphics to illustrate the point.

The most pronounced ST/T wave abnormality is found in lead V2. It’s difficult to tell because the QRS complexes run into one another, but the S wave is extremely deep in lead V2, possibly as deep as 35 mm (blue arrows). With LVH, you should expect the lead with the deepest S wave to show the most ST segment elevation and/or T wave height!
The red curve shows the upward concavity of the ST segment, which is another common finding with LVH. I have seen upwardly convex ST segments with LVH, but it’s rare, and it always makes me suspicious of acute anterior STEMI!
I’ve outlined the shape of the T wave with orange lines. You can see that the T waves are asymmetrical, another finding consistent with a “strain pattern” or depolarization abnormality with LVH.

In the left precordial leads, the most most pronounced ST/T wave abnormality is found in lead V5. Again, it’s difficult to discern because the QRS complexes run into one another (as they often do with LVH) but the height of the R wave may be as high as 30 or even 40 mm (blue arrows).
The red curve shows the downwardly concave ST segment depression (exactly opposite the right precordial leads).
I have outlined the T wave inversion with orange lines to show the asymmetry. Again, a common finding with “strain patterns” or depolarization abnormalities with LVH.



Example #1.

This is an atypical “strain pattern” with many typical features.
I suspect the possibility that leads V1 and V2 might have been accidentally transposed but that doesn’t really matter. For the purposes of STEMI recognition, the typical features outweigh the atypical features.
In the first place, you should immediately notice the “widened QRS-T angle” that is the hallmark of a secondary repolarization abnormality. You will notice the same finding for LBBB and paced rhythm!
Importantly, the degree of the secondary ST-T abnormality is, generally speaking (there are some caveats), proportional to the size (or amplitude) of the QRS complex in the opposite direction!
If you take nothing else away from this post, please learn this “trick”.

Herein lies a problem with prehospital 12-lead ECGs!
With left ventricular hypertrophy (LVH) the QRS complexes are often “cut off” at the top or bottom or they run together with other QRS complexes which can create the illusion that the QRS complexes are smaller, so you have to train your eye!
Take a look at this ECG and find the most severe ST-T wave abnormality.
That’s easy! Lead I clearly shows the most pronounced ST-T wave abnormality. The ST-segment is depressed, downwardly concave, and shows a deep inverted T-wave.
Does the amplitude of the R-wave in the opposite direction explain it? No way! It’s even smaller than the QRS complex in lead II, and the ST-T wave abnormality in lead II isn’t nearly as severe!
What is the second-worse ST-T wave abnormality? Lead V3! Does the depth of the S-wave in the opposite direction explain it? Not really.
But wait! Are we certain we’re getting an accurate “read” on the amplitude of the R-wave in lead I and the depth of the S-wave in lead V3?
I’m not so sure!

I suspect the possibility that the computer is “cropping” the QRS complexes to fit them on the ECG paper. See the little horizontal line that marks the “top” and “bottom” of these QRS complexes?
I’ve seen it many times before!
So ask yourself this question:
Generally speaking, does there seem to be a relationship between the QRS-complex and the degree of ST-elevation or depression in the opposite direction?
If the answer is “Yes!” then don’t call the STEMI Alert. Instead, perform serial ECGs and look for changing ST-segments and T-waves! ST-segments and T-waves shouldn’t “evolve” or change over time if it’s a simple secondary ST-T wave abnormality!
Example #2

ST segment morphology

check out this post... on ST segment morphology
http://ems12lead.com/2009/06/04/st-segment-morphology/


Because acute myocardial infarction (STEMI) is not the most common cause of ST segment elevation in chest pain patients, we need to consider other factors like reciprocal changes to shore up the diagnosis.
It’s also a good idea to be well versed in the typical appearance of the STE-mimics (paced rhythms, left ventricular hypertrophy, benign early depolarization, pericarditis, left ventricular hypertrophy, hyperkalemia, and so on).
Another factor that can assist you is an analysis of the morphology of the ST segment.
The normal ST segment should not be flat. It should have an upward concavity sometimes referred to as a “take-off”.
When an ST segment loses its concavity and becomes straight or upwardly convex, it can indicate acute myocardial infarction.
Consider this image from WJ Brady, SA Syverud, C Beagle et al. Electrocardiographic ST-segment Elevation: The Diagnosis of Acute Myocardial Infarction by Morphologic Analysis of the ST Segment Acad Emerg Med 2001; 8(10):961-967

You can draw an imaginary line between the J point and the apex of the T wave. If the ST segment is below that line, then it’s upwardly concave. If it’s even with or above that line, then it’s “non-concave” (straight or upwardly convex) which is suspicious for acute myocardial infarction.

(Note: As I learned on Facebook on 12/22/2010 this phenomenon was described in Pardee HEB. An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 1920; 26: 244– 257 and referred to as “coving” of the ST-segment.)

If it helps you to remember, an upwardly concave ST segment makes a “smiley face” (good) and an upwardly convex ST segment makes a “frowny face” (bad).

Does that mean that acute myocardial infarction always presents with non-concave ST segments when ST segment elevation is present?

Not at all! This finding is not particularly sensitive. It is, however, fairly specific. When non-concave ST segments are present, it’s another piece of the puzzle.
The STE-mimics almost always present with upwardly concave ST segments and an absence of reciprocal changes.
*** NOTE: Dr. Smith from Dr. Smith’s ECG Blog disputes this claim and has shown me a couple of cases of left ventricular hypertrophy with upwardly convex ST-segments in the right precordial leads that were not experiencing STEMI. ***
You might have noticed that I used the phrase “upwardly concave” as opposed to simply “concave”.
That’s because “concave” is “convex” depending on your perspective. That’s why I always mention the direction of the concavity or convexity.
Sometimes this can get confusing! Consider this image from the AHA’s new STEMI book.

The caption says “concave down” even though it’s referring to an ST segment that is upwardly concave. This may have been a typo, but I think it’s always helpful to use standardized definitions/language when it comes to medicine (or incident command)!

Regardless, if you look at this image from the STEMI book, the second window shows ST segments with a loss of upward concavity (ST segment straightening) and hyperacute T waves.
After PCI, you can see the development of Q waves and terminal T wave inversion (which usually indicates a STEMI that’s been around for a while).
It’s tough when a chest pain patient presents with an ECG with ST segments like we see in the third window. It’s often difficult to determine the age of an ECG abnormality like that.

Axis determination

This one is a really good video for axis determination....very simple and to the point...Thanks Christopher..:)

Axis determination

http://www.youtube.com/watch?feature=player_embedded&v=kOdk20FgcC0

so now its soo easy to tell the axis by just looking at Lead 1, aVf and lead 2.....:)

Adding few other facts....
aVr : always negative...
Pwave in Lead 1 is always positive...
if not then lead placement is wrong for sure....