Showing posts with label ECG/EKG Archive. Show all posts
Showing posts with label ECG/EKG Archive. Show all posts

ECG: 40 y/o Female with Chest Pain

Adam Thompson, EMT-P | 10:49 PM | , | 26 comments

Also Posted over at ECG Experts

Submission thanks to Tim Waters, CCEMTP of Lee County Medstar

40 yo female, thin build with no history/meds/allergies. + smoker. Works as painter outside and was painting when developed pain in her upper chest/left arm which is the same she uses to paint. Also adds that she has been moving and lifting numerous heavy objects over the past week and since then has been having these episodes of shoulder discomfort. Pain is non-radiating with moderate reproducibility with movement and inspiration. I forget what severity scale she gave it but was definitely uncomfortable. Onset was about 3 ½ hours prior to presentation while painting with her trying to work through the pain until it became to unbearable.. Denies nausea, is diaphoretic but has been working outside.



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 

66 year old male CC: Chest pain

Tom B | 1:09 PM | | 3 comments

Here's another great case submitted by Nick Ciaravella of Grady EMS in Atlanta, GA.

66 year old male presents to EMS with chest pain.

S - Chest Pain
A - None
M - Atenolol, HCTZ
P - HTN
L - meal, 7 hours prior to event
E - Mowing his lawn

O - Started while mowing his lawn
P - Provoked while exerting himself, Palliated initially when he sat down to rest
Q - Sharp
R - Substernal, initially radiating to his jaw, when he rested the pain was only in his chest
S - Initially 10/10, upon ems arrival 4/10, en route 8/10, 9/10, and 10/10 upon arrival at ED
T - No previous episodes

The patient initially presented to EMS with 4/10 pain and vitals as follows, 148/84, pulse 72, 18 respirations, SPO2 96%, Lung sounds clear and equal, BGL 103.

The patient was placed on 3 LPM O2 via NC, given 324 mg Aspirin PO, given 0.4 mg Nitro Tablet Sublingual and then 1 inch of Nitro Paste Transdermal. The Patients pain increased en route to the ED and began to radiate down his left arm en route.

12-lead ECG #1


12-lead ECG #2 (about 15 minutes later)


What do you think?

See also:

Anterior ischemia or posterior STEMI?

26 year old male CC: Chest pain

74 year old male CC: Chest pain

50 year old male CC: Respiratory distress, chest pain

48 year old male CC: Chest discomfort, shortness of breath

Pure (Isolated) Posterior STEMI -- not so rare, but often ignored! - Dr. Smith's ECG Blog

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)

67 y/o male CC: Syncope

Adam Thompson, EMT-P | 1:10 PM | , | 12 comments



Also posted over at 12-Lead ECG Blog, go check out all the other great stuff there!


A 67 y/o male has fallen to the ground at his residence. His "partner" called 911 after seeing that he was unconscious. Upon your arrival the patient is alert and requesting that you pick him up because he really needs to make a bowel movement. The patient denies syncope but states that he does not remember falling.

Here is the initial ECG and the subsequent 12-lead ECG. Sorry for the poor quality.





What do you see?

What do you want to know?

What do you want to do?



****Update****



His Vital Signs

HR correlates with monitor, pulse not palpable at radial.

Initial BP 78/60

AAOx3, normal mental status, just wants to make a bowel movement.

Skin - Pale, more pronounced and white from the waste down. Skin was relatively dry.




****Update 5/20/2010****


A new 12-lead ECG is captured during transport.

The patient's vital signs do not improve dramatically with IV fluids.




****Update 5/23/2010****

During transport the patient's condition declined rapidly. After the 12-lead ECG above was captured, the patient went in to a decorticate posture. As most of you know, this is indicative of some sort of neuro compromise. With his airway control, mental status, and respiratory rate all declining, brainstem herniation was at the top of the list of differentials.

The patient became pulseless and apneic just prior to arriving at the ER--according to my partners, just after he released the bowel movement. The patient was not revived.

So what happened here?

Me and the field training officer came up with a few possible solutions. First, there is ST-elevation in the inferolateral leads of the initial 12-lead ECG. With the hypotension, a RCA occlusion is a possibility. If the patient has a dominant RCA, there appears to be some ST-depression in the septal leads, but this is a RBBB pattern, so with the T-wave discordance, the ST-depression is not a good clinical indicator of posterior wall involvement.

First Possibility: Right-sided infarct with hemodynamic compromise leading to a syncopal episode. The syncope caused a secondary head injury which cerebrally herniated during transport. I would like to note that this is highly unlikely. Also, the patient did not improve with fluids, which would have happened with a traditional RV infarct.

Second Possibility: It is much more likely that the patient had an atypical hemorrhagic stroke that presented with the first symptom of syncope. The changes on the 12-lead ECG could just be concurrent with cerebral ischemia. This is not completely understood, but theories involving nerve endings in the myocardium are abundant. The patient's ICP would have increased during transport with the final result being cardiac arrest.

Third Possibility: Abdominal aortic aneurism with severe secondary cerebral ischemia due to hemodynamic instability. I'm not fond of this idea even though the AAA fit the picture in the beginning, it does not explain the decorticate posturing.


We also keep the huge possibility that we have no idea what happened on the list. Ok, so I wish I had more to give you, but an autopsy was not performed on this patient. It remains a mystery.

26 year old male CC: Chest pain

Tom B | 6:56 AM | | 2 comments

Here's a great case submitted by a faithful reader who wishes to remain anonymous.

EMS is called to a 26 year old male complaining of chest pain.

On arrival patient is found sitting on his living room couch. He appears anxious and acutely ill.

He states that he was riding his bike when he became anxious, had a "coughing spell" and started to experience chest discomfort. The location of the chest discomfort is in the center of his chest and slightly to the left.

Onset: Sudden while riding a bike
Provoke: Nothing makes the pain better or worse
Quality: Difficult to describe but with prompting the patient calls it "pressure"
Radiate: Left jaw and left arm
Severity: 7/10
Time: No previous episodes

The patients skin is warm and moist. The color is normal.

The patient denies shortness of breath. Breath sounds are clear bilaterally.

He is nauseated but he has not vomited.

Past medical history: Healthy

Medications: None

Vital signs are assessed.

Resp: 22
Pulse: 98
BP: 140/84
SpO2: 100 with oxygen via NRB @ 15 LPM

The cardiac monitor is attached.


A 12-lead ECG is captured.


What is your impression?

*** Update 05/14/2010 ***

The importance of serial ECGs cannot be over-emphasized.

In this case, a second 12-lead ECG was captured just prior to arrival at the hospital.

Does this new information shed any light on the probably diagnosis?


What else could you have done?

Strip Tease 15

Adam Thompson, EMT-P | 5:38 PM | | 1 comments

What is "The Strip Tease"?


Click Here to find out.







Please provide your impressions of the ECG strip in the comments section.

Discordant ST-Segment Elevation in LBBB or Paced Rhythm

Tom B | 11:23 AM | , , | 0 comments

If you've been following the Prehospital 12-Lead ECG blog for a while, you know that I'm advocate of using Sgarbossa's criteria to help identify acute STEMI in the presence of left bundle branch block (LBBB) or paced rhythm.

According the Sgarbossa's original criteria, 5 mm of discordant ST-segment elevation is required to identify AMI in the presence of LBBB.

Why 5 mm when normally we require only 1 or 2 mm of ST-elevation?

Because in the setting of left bundle branch block or paced rhythm, it's normal for the ST-segment and T-wave to be defected opposite the main deflection of the QRS complex!

That's why it's necessary to consider the depth of the QRS complex when examining the amount of discordant ST-segment elevation. The deeper the S-wave, the greater the secondary ST-T wave abnormality in the opposite direction!

In the original article I wrote on the topic, I showed this example 12-lead ECG to show why the 5 mm criterion is problematic.



As you can see, this 12-lead ECG shows sinus rhythm with left bundle branch block and > 5 mm of discordant (opposite the QRS complex) ST-elevation in leads V1, V2, and V3 (the right precordial leads). The T-wave are huge!

The problem is, this patient was not experiencing acute myocardial infarction. The ST-segments are elevated > 5 mm because the S-waves are extremely deep (off the bottom of the ECG paper for leads V2 and V3).

Had we used the modified criterion of discordant ST-elevation that is = or > to 0.25 the QRS complex (credit to Dr. Smith), we would have seen that in lead V1 the S-wave is 50 mm deep. Thus, we would require at least 12.5 mm of ST-segment elevation to consider this finding positive for acute STEMI.

There's another way the modified criterion can help you!

Consider this 12-lead ECG that shows a ventricular paced rhythm. It's been in my collection for many years, and I regret that I no longer recall where it came from.



This ECG does not meet Sgarbossa's criteria for diagnosing AMI in the presence of LBBB. With the exception of lead V6, the paced QRS complexes show appropriate T-wave discordance, and none of the ST-segments are elevated to 5 mm or more.

But wait! The ST-segments are elevated far greater than 0.25 the depth of the QRS complex in leads II, III, and aVF! This patient is experiencing acute inferior STEMI!

The intrinsic QRS complex in the right precordial leads also shows an > R/S ratio in lead V1 and V2 and ST-segment depression suggesting posterior extension, which clinches the diagnosis.

So remember, when using Sgarbossa's criteria, huge QRS complexes can cause false positive and tiny QRS complexes can cause false negatives, unless you use the modified rule that considers ST-segment elevation as a percentage of the QRS complex!

See also:

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graph

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

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

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

Tom B | 11:13 AM | | 0 comments

Cross-posted to the Prehospital 12-Lead ECG blog and 12-Lead ECG (Cardiography & Electrocardiography Experts)

In the January 2010 EMCast at EMedHome.com, Amal Mattu MD reviews Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27:916-921.

His comments confirm what I have suspected for a long time with regard to LBBB in the setting of suspected ACS.

"This is a really interesting and provocative article that may bust the traditional myth that we should be thrombolysing or cathing everybody with chest pain who presents with a new left bundle branch block."

"They found that there was no significant difference in the rate of acute myocardial infarction between patients that were presenting with a new, or presumed new left bundle branch block pattern versus patients with a known old left bundle branch block pattern […] In other words, when patients presented with a new left bundle branch pattern, those patients did not rule-in at any greater increased frequency compared to the other patients, and based on this data the argument is certainly made that when patients have chest pain and they present with the left bundle branch block pattern, there’s not necessary a need purely based on the presence of a new left bundle to assume that that patient is having an acute MI, and therefore that patient needs to get thrombolytics or go immediately to the cath lab."

"As I mentioned before, there is reasonable data to indicate that if the patient has a left bundle branch block – whether it’s new or old – and they demonstrate Sgarbossa criteria, then those patients do end up ruling-in for acute myocardial infarction […] Simple presence of a new left bundle branch block pattern does not appear to warrant immediate activation of the cath lab or immediate thrombolytics according to this study."

Amal Mattu MD does add the caveat that the guidelines still state that patients with new LBBB are supposed to get reperfusion therapy.

See also:

Identifying AMI in the presence of LBBB

False positive cardiac cath lab activations

Review of Factors Associated With False-Positive Emergency Medical Services Triage for Percutaneous Coronary Intervention

Sgarbossa's criteria - new graph

Strip Tease 14: Answer

Adam Thompson, EMT-P | 11:05 PM | | 4 comments



This is simply artifact.

I used the calipers to map the RR interval. By doing this you can see which complexes are conducted beats and which are artifact.

It would be highly unlikely for a narrow complex tachycardia to have a rate of 300 outside the presence of an accessory pathway.

P waves are present but difficult to make out with presence of artifact.

A simple way to conclude the presence of artifact is by checking for a mechanical pulse.




Addition by Rogue Medic 00:17 9/18/09.

My little bit of strip marking to show what I was looking at with this strip. These are just different ways of coming to the same conclusion. In EMS there is rarely just one right way of doing things. The response of the patient is the best indicator of what is right. Sometimes nothing is right.




.

Strip Tease 14

Adam Thompson, EMT-P | 11:01 PM | | 5 comments


Click above for an understanding of where these came from and how they work.


Please provide your impressions of this ECG strip. Leave comments. You will not be chastised for misinterpretation, and I greatly appreciate participation.

Dextrocardia

Adam Thompson, EMT-P | 5:41 PM | , , , | 8 comments

Dextrocardia



A condition less known...


Dextrocardia situs inversus refers to a condition in which the heart is a mirror image of normal placement. With dectrocardia the main mass of the heart sits right of the mediastinum. When all visceral organs are mirrored the condition is dextrocardia situs totalis.

Dextrocardia occurs in approximately 1 in 12,000 people (according to wikipedia).


The above chest X-ray is not reversed, that is a patient with dextrocardia.
All of the heart chambers and great vessels are reversed, as seen above.
Left Ventricle (LV), Right Ventricle (RV), Left Atrium (LA), Right Atrium (RA), Pulmonary Artery (PA), Aorta (Ao).

Above is a comparison of a normal heart and the heart of a patient with dextrocardia


As you can imagine, there are multiple ECG changes found on the patient with dextrocardia. If you know the patient has this condition, it may be in your best interest to mirror normal electrode placement.

Take a look at some 12-leads of dextrocardic patients below:





Notice the obvious change in axis. A negatively deflected lead I would indicate right axis deviation. When leads II & III become deflected in addition, this would indicate extreme right axis deviation (ERAD). ERAD is most often seen when impulses originate in the ventricles as with ventricular tachycardia, or ventricular pacemakers. ERAD may appear with dextrocardia.

When you see a negative QRS in lead I, and a positive QRS complex in aVR, you should first suspect misplaced leads. If they are placed correctly, dextrocardia should enter your differential.
Common ECG findings:

not all of these are always present

- Global negativity in lead I, (a negative p wave, QRS, and negative T wave).

- Positively deflected QRS in aVR

- Negative p wave in lead II

- Reverse R wave progression in precordial leads


Causes of Dextrocardia:

- Marden-Walker Syndrome: A rare genetic disorder characterized by blepharophimosis, joint contractures and fixed facial expression.

- Kartagener syndrome: A rare genetic disorder characterized by enlarged bronchial tubes, sinusitis and cross-positioning of body organs.

- Campomelia Cumming type: A rare syndrome characterized by limb and multiple abdominal organ abnormalities. The disorder results in death before birth or soon after.


Things to consider:

So, if you ever have the idea that the ECG you are looking at, looks as if your leads are all reversed, maybe the heart is.

When defibrillating these patients, traditional pad placement should be mirrored to the right chest. Anterior/posterior placement should be just right of the mediastinum.


Strip Tease 13: Answer

Adam Thompson, EMT-P | 5:28 PM | | 7 comments

This was an AVB example provided by my training captain in a class that he taught.

Most people will call this a 3:1 2nd degree type 2, or Mobitz 2.

Lets have a look:

First measure your PP interval, and make sure they "march out"

Okay, seems like the PP is pretty consistent. There are 3 p-waves for every R -wave; this favors third degree AV block. Now lets check the RR-interval.

As expected the RR-interval is consistent. This is also highly favorable of third degree AVB, but isn't conclusive. We have to prove complete atrioventricular(AV) disassociation. We do this by measuring our PR-intervals.
If you measure the first PR-interval against the last PR-interval you will see that they do not match. This leads to a couple conclusions.

Either this is a 3rd degree AVB and the atrial rate just happened to be almost exactly 3 times as much as the ventricular rate. If this is true, further monitoring will show the AV disassociation clearer, since the PR-interval is varying.

Or, this is a high grade transient AVB. Meaning this is the end of a Mobitz 2, as it becomes a 3rd degree AVB. I call these Mobitz 3s.

I personally think this is a simple 3rd degree AVB and coincidence confused the masses. If all else fails, and the pattern continues, call it a 3:1 AVB.

ps. If you don't have a fancy set of calipers, a piece of paper works fine. Just draw lines on the pice of paper to measure out your intervals and see if they match.

Strip Tease 13

Adam Thompson, EMT-P | 12:31 PM | | 6 comments


Provide your impressions within the comments.

Long QT Syndrome Part II

Adam Thompson, EMT-P | 3:19 PM | , | 3 comments


What is Long QT Syndrome?

Long QT Syndrome (LQTS) is a condition purely diagnosed by an electrocardiogram (ECG). This condition is represented by a long QT interval, hints the name. This represents delayed ventricular repolarization. This condition can be genetic or induced by certain prescribed medications.

How do I detect it?

Easy, as the name implies, measure the QT/QTc interval. The image below shows that the QT interval begins at the very end of the PR Interval, where your isoelectric line will begin another positive or negative deflection, and it ends at the very end of the T wave. Lead II is generally a good place to make your measurement. This may change depending on the R axis.


Normal QT intervals are between 300 & 450ms (0.30 - 0.45 seconds)

An easier way to measure is by looking at your 12-lead diagnostics. While rhythm interpretation may not always be up to par with your monitor; the measurements are usually pretty accurate.



What is the difference between QT & QTc?

The c in QTc stands for corrected. The QTc is the QT interval with a formulated correction based on the patient's heart rate (HR). The faster the HR the shorter the QT interval. The QTc may not always be accurate, but is commonly used for diagnostic purposes. Bazett's formula is used to determine QTc (well according to wikipedia it is).

Why is LQTS bad?

Remember the term refractory period?

Here is your refresher:

The absolute refractory period is the interval during which a second action potential absolutely cannot be initiated, no matter how large a stimulus is applied.

The relative refractory period is the interval immediately following during which initiation of a second action potential is inhibited but not impossible.[1]


Well people with LQTS have a prolonged refractory period, this includes a prolonged relative refractory period. As the definition explains, the relative refractory period tries not to but may invite pre-excitation. What this means is that another beat, from another part of the heart, may occur.

One example of aberrancy due to abnormal refractory period is Ashman's phenomenon. This is an arrhythmia with what is called a "long-short cycle". In atrial fibrillation, you may see a string of QRS complexes with longer R-R intervals (long cycle) followed by a PVC or a run of what looks to be PVCs. This will be followed by QRS complexes with shorter R-R intervals (short cycle). This is caused by pre-excitation during the relative refractory period, and the "PVC" is actually an aberrantly conducted supraventricular complex (bundle branch block pattern). The conduction was delayed due to a busy electrical pathway. Picture a traffic jam in the hearts one lane electrical highway. Below is an example, look at the R-R intervals pre & post premature beat.


Another complication of a longer refractory period is what is known as R on T Phenomenon. This condition may be more severe because it may interfere with hemodynamic stability. A premature complex finds it's home on the tail end of a supraventricular complex and takes over. While the ventricles are attempting to repolarize another focus decides he wants to take over. The best way to do this is by depolarizing while the other pacemaker is repolarizing. Like attacking a sleeping enemy. Below is another image stolen from Google. Those complexes are ventricular in origin.


Another risk associated with LQTS is sudden cardiac arrest. That one doesn't need much explanation. The cause is most likely an arrhythmia brought on by the R on T phenomenon.


More on LQTS to come. If any information I have provided is thought to be inaccurate, please let me know (Tom). I have no problem with being wrong, there is a first time for everything (hopefully sarcasm was detected).



*Once again, all images stolen from Google searches.

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