You respond to a 72 y/o female complaining of shortness of breath. Upon arrival you find an average sized elderly female with tachypnea and pale, moist skin. She states that she can’t do anything without feeling very short of breath. This is the ECG you obtain on the patient, what are you thinking at this point?
Watch the video below for the full case review and interpretation.
You respond to a 65 y/o Male at his residence. His daughter, on scene, called 911 because she is worried about her father’s health. She states that he just hasn’t been acting right. “He is weaker than normal, and becomes short of breath very easily”. The patient himself is not thrilled about your presence. He is a rather obese man (about 400 lbs), and he is sitting in his recliner sans shirt or pants. His immediate area provides evidence that he doesn’t move
S – The patient states that he is always weak and it is normal for him to get short of breath when he gets up.
A – NKDA
M – Glucophage, Gabapentin, Albuterol, Singulair, Prevacid, Carevedilol, Enalapril, Digoxin, Aspirin, Oxygen
P – AMI, CHF, Asthma, Non-insulin dependent diabetes, AICD
L – Oreos and Orange Juice
E – Sitting in his chair
B/P: 61/37, Left Arm
SpO2: 83, on 2 lpm O2,
Pulse: 40 & regular
Resp: 30 & regular
Skin: Pale, cool, & clammy
You place your patient on the monitor and obtain the following 12-lead. What would you immediately ask your patient? What is your interpretation of the ECG? What treatments would you provide?
I’ve been at it again with the video tutorials. Here is a quick, two-part explanation of Bundle Branch Blocks. I explain what causes the ECG changes associated with bundle branch blocks to the best of my abilities within the short amount of time that Youtube allows.
Did you know that both types of bundle branch blocks require you to look at more than just lead V1 to truly identify them? If not, make sure you see part 2.
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.
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.
*It is important to remember that there are many tachycardic arrhythmias that could cause syncope as well.
Acute Myocardial Infarction
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.
From Dr. Amal Mattu:
• 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)
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
• 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
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:
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)
• 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
• Placement of an ICD is the only effective treatment
• Antiarrhythmic drugs (including beta blockers, amiodarone, etc.) ineffective
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)
• 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
• Beta blockers, calcium channel blockers to improve LV filling and diastolic \function ]
• Amiodarone if ventricular dysrhythmias present
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?
Pure (Isolated) Posterior STEMI — not so rare, but often ignored! – Dr. Smith’s ECG Blog
62 year old male presents to the emergency department complaining of chest discomfort.
** 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.
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?
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)