Amal Mattu on EKGs: ST elevation, Wide Complex Tachycardia and PE

Source:http://ercast.libsyn.com/

Emergency cardiology master  Dr. Amal Mattu  gives the low down on ST elevation, T-wave inversion and bizarre, wide-complex tachycardia.

Basic Rules of ST elevation

1.        No matter how good the rules, nothing is 100% certain

2.       15-20% of STEMI cases sent to the cath lab will have clean coronaries

3.       Always obtain and OLD EKG if possible

4.       Positional and pleuritic chest pain is present in 15% of True ACS

A Stepwise approach to distinguishing pericarditis vs STEMI vs Early Repolarization

Disclaimer-This process is not 100% but will pick up the majority of MI.

The first part of the process is to look for the life threat. In this case, STEMI.

Step 1: Look for findings that clearly define STEMI. When reading the EKG...

•  Is there any ST segment depression in the other leads leads (except AVR and V1-nonspecific). These are  “reciprocal changes” and strongly suggest STEMI over other causes of ST elevation.
•  Look at the ST segment elevation in Leads II and III. If the ST elevation in lead III is greater than in lead II, think STEMI. Early repolarization and pericarditis should not have more ST elevation in lead III compared to lead II.
•  Look at the morphology of ST segment elevation. Concave upward (as in a cup holding water) does not rule out STEMI. If morphology is horizontal (tabletop) / convex upward (tombstone), think STEMI.
•  Serial EKGs show increasing size of Q waves ( make sure they are new Q waves) = STEMI

Step 2: Look for findings that define pericarditis

PR depression in multiple leads >2mm. But be warned, PR depression is not only seen in pericarditis. It  can also be seen in STEMI, so don’t hang your hang your hat on it. PR depression is also transient. It can last from a few hours up to two days and is most associated with viral pericarditis than other types of pericardial inflammation.

Step 3: If there is still a question as to what’s causing the ST elevation...Perform or order an ECHO

Pericarditis-may have fluid. MI-may have wall motion abnormality. Benign early repol will be normal. Unfortunately, pericarditisSerial troponins may help, but what really helps is an old EKG.

 Pulmonary Embolism and T-wave inversion

•  T- wave inversions are not just caused by cardiac ischemia and, in the setting of PE, may be more prevalent than sinus tachycardia. The most common place to find T wave inversions in PE are leads V1, V2, V3. There is no mystery as to why it should be these leads - a large PE can cause acute pulmonary hypertension which will be seen as changes in the anteroseptal leads.
• If you see new T-wave inversions in anterior septal leads V1, V2, V3 and the inferior leads(II, III and AVF), that equals new pulmonary hypertension and your suspicion of PE should be even higher -this is a PE until proven otherwise.
•  The classic teaching is that most PEs will present with sinus tachycardia, but in the large studies, it’s only found in 30-50% of confirmed cases of PE.  Respiratory rate and history are better predictors of PE than sinus tachycardia.

Hyperkalemia and its effect on EKGs

Amal’s Axioms

• A bizarre, wide complex, EKG equals hyperkalemia until proven otherwise. Think of hyperkalemia as the EKG’s great imitator- the syphilis of electrocardiography. Hyperkalemia produces widening of the QRS and, as the K level goes up, the p waves start to disappear.  The EKG in this setting can resemble V-tach, ST segment elevation, fascicular blocks. Hyperkalemia can do pretty much anything to an EKG.
• Ask yourself, is the wide complex rhythm over 120bpm? To be diagnosed as ventricular tachycardia, the rate should be over 120 unless the patient is  already on an antidysrhythmic like amiodarone.
• If your patient has a wide complex rhythm that you can’t figure out, but think there may be hyperkalemia, there is little risk in giving a few amps of bicarb (1-2 amps as a trial- bicarb is quickly eliminated by the body) or calcium ( 1-2 amps of gluconate is safe even in dig toxicity).
•  A sodium channel blocker overdose (e.g. tricyclic antidepressant or cocaine) can also cause a wide complex, bizarre EKG.  If a patient has hyperkalemia, a tricyclic antidepressant  or cocaine overdose, do not use an antidysrhythmic like amiodarone or procainamide -they will potentiate the toxic effect.  The sodium channels are already poisoned and amiodarone/procainamide will just make things worse.

Interview with Amal Mattu
By Rob Orman
Written summary by Justin Arambasick, Rob Orman

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ECG-Myocardial Infarction

Source: ABC of ECG (BMJ)


Hyperacute T waves
The earliest signs of acute myocardial infarction are subtle
and include increased T wave amplitude over the affected area.
T waves become more prominent, symmetrical, and pointed
(“hyperacute”). Hyperacute T waves are most evident in the
anterior chest leads and are more readily visible when an old
electrocardiogram is available for comparison. These changes
in T waves are usually present for only five to 30 minutes after
the onset of the infarction and are followed by ST segment
changes.


ST segment changes
In practice, ST segment elevation is often the earliest recognised
sign of acute myocardial infarction and is usually evident within
hours of the onset of symptoms. Initially the ST segment may
straighten, with loss of the ST­T wave angle . Then the T wave
becomes broad and the ST segment elevates, losing its normal
concavity. As further elevation occurs, the ST segment tends to
become convex upwards. The degree of ST segment elevation
varies between subtle changes of < 1 mm to gross elevation of > 10 mm.



Pathological Q waves
As the acute myocardial infarction evolves, changes to the QRS
complex include loss of R wave height and the development of
pathological Q waves.
Both of these changes develop as a result of the loss of
viable myocardium beneath the recording electrode, and the
Q waves are the only firm electrocardiographic evidence of
myocardial necrosis. Q waves may develop within one to two
hours of the onset of symptoms of acute myocardial infarction,
though often they take 12 hours and occasionally up to 24
hours to appear. The presence of pathological Q waves,
however, does not necessarily indicate a completed infarct. If
ST segment elevation and Q waves are evident on the
electrocardiogram and the chest pain is of recent onset, the
patient may still benefit from thrombolysis or direct
intervention.
When there is extensive myocardial infarction, Q waves act
as a permanent marker of necrosis. With more localised
infarction the scar tissue may contract during the healing
process, reducing the size of the electrically inert area and
causing the disappearance of the Q waves.



Resolution of changes in ST segment
and T waves
As the infarct evolves, the ST segment elevation diminishes and
the T waves begin to invert. The ST segment elevation
associated with an inferior myocardial infarction may take up to
two weeks to resolve. ST segment elevation associated with
anterior myocardial infarction may persist for even longer, and
if a left ventricular aneurysm develops it may persist indefinitely.
T wave inversion may also persist for many months and
occasionally remains as a permanent sign of infarction.



Reciprocal ST segment depression

ST segment depression in leads remote from the site of an
acute infarct is known as reciprocal change and is a highly
sensitive indicator of acute myocardial infarction. Reciprocal
changes are seen in up to 70% of inferior and 30% of anterior
infarctions.
Typically, the depressed ST segments tend to be horizontal
or downsloping. The presence of reciprocal change is
particularly useful when there is doubt about the clinical
significance of ST segment elevation.

Reciprocal change strongly indicates acute infarction, with a
sensitivity and positive predictive value of over 90%, though its
absence does not rule out the diagnosis.
The pathogenesis of reciprocal change is uncertain.
Reciprocal changes are most frequently seen when the infarct is
large, and they may reflect an extension of the infarct or occur
as a result of coexisting remote ischaemia. Alternatively, it may
be a benign electrical phenomenon. The positive potentials that
are recorded by electrodes facing the area of acute injury are
projected as negative deflections in leads opposite the injured
area, thus producing a “mirror image” change. Extensive
reciprocal ST segment depression in remote regions often
indicates widespread arterial disease and consequently carries
a worse prognosis.

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ST Elevation

Knowledge

The ST level is measured relative to the PR interval. While the U-P level theoretically would be preferred it cannot be used because it disappears with tachycardia. When there is a short PR interval, it can be particularly difficult for computer algorithms to find the isoelectric reference level. The direction of the ST vector and the relative position of the electrode measuring the vector determine whether the ST amplitude is positive (elevation) or negative (depression). For instance at rest, since the main ST vector projects along the long axis of the heart toward the apex, AVR will register a negative ST amplitude and V5 will register a positive ST amplitude (early repolarization). With tachycardia or ischemia the direction changes, as does the ST amplitude. As for any vector shift that is perpendicular to an electrode, no amplitude will be registered. Pathological processes that cause ST elevation shift the entire vector from it's long axis of the heart orientation and move it through the area of inflammation (pericarditis) or transmural ischemia (infarction or spasm). Thus, pathological ST depression does not localize but reflects a global subendocardial process while pathological elevation occurs directly over the involved area. It is important to determine if the ST elevation was documented on previous ECGs and if the ST level is currently changing or is stable. Acute or dynamic ST elevation can be due to severe transmural ischemia secondary to thrombus, spasm or a tight fixed coronary artery lesion or a combination of these situations. It can be the first ECG manifestation of an evolving myocardial infarction and it represents the ECG criteria for thrombolytic therapy. However, if the pain does not persist, it more likely is due to variant or unstable angina. The elevation localizes the ischemic lesion to the coronary artery supplying the area of myocardium reflected by the ECG leads. It represents transmural ischemia and is very arrythmogenic. Chronic or persistent ST elevation could be due to an aneurysm when it occurs over Q waves or to chronic pericarditis (i.e., with uremia), but it most commonly occurs with a normal ECG pattern and is known as early repolarization. It may actually be due to late depolarization and is a very normal finding even to 3-4 mm in amplitude. Normally early repolarization lessens with increases in heart rate while ischemic ST elevation increases.

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Recommendations

If the ST elevation has been present on prior ECGs: If the ST elevation has been present on prior ECGs, the ECG does not exhibit diagnostic Q waves (no Q wave is wider than 35 millisec or 25% larger than the following R wave), and the elevation lessens with increases in heart rate then the benign finding of early repolarization is probable. The ECG with this finding usually will be obtained in a healthy, asymptomatic individual but it can also be obtained in a patient presenting with non-cardiac chest pain or with complaints due to another pathological process which makes the diagnosis more complicated. In this later circumstance, the early repolarization does not rule out a cardiac process but makes other diagnoses more likely. If the ST elevation has been present on prior ECGs and occurs over diagnostic Q waves (Q wave wider than 35 millisec and 25% larger than the following R wave), a LV aneurysm or large wall motion abnormality is likely. In the case of an anterior location (i.e., V1-4), an abnormal precordial movement may be noted on examination. An echocardiogram would be the best way to evaluate LV function to see if an ACE inhibitor or other vasodilator was necessary to improve survival and lessen admissions for CHF. When the ST elevation is a new finding: The patient must be carefully questioned regarding ischemic symptoms including angina pectoris, chest pain, and shortness of breath, chest squeezing or pressure. q      If the symptoms are consistent with myocardial ischemia, an aspirin and nitrates should be given immediately. If due to coronary spasm, the symptoms and elevation should resolve. If they do not, then thrombolysis should be given unless there are contraindications (bleeding disorder, recent stroke, operation or bleeding, etc). Enzymes should be drawn but treatment need not be delayed for their analysis. The ECG often also exhibits increased R and T wave amplitudes and the elevation usually is in the area of the coronary artery with spasm or thrombus. q      If the patient's pain is pleuritic and positional, then consider pericarditis. A history of a URI or pneumonia, prior pericarditis, auto-immune disease and arthritis support the diagnosis of pericarditis. Physical exam may reveal a multi-component rub. ECG findings that also support pericarditis are PR depression, low amplitude T waves and ST elevation in multiple areas. If diagnosed, laboratory studies are indicated including renal function for uremia and patients should be closely followed for cardiac tamponade (distant heart sounds, narrow pulse pressure, pulsus paradoxus, hypotension). Echocardiography and cardiology consultation is usually indicated. q      If the patient is asymptomatic, then the most likely diagnosis is Early Repolarization. To confirm this, the ECG can be repeated to see if the pattern is stable. "Silent Ischemia" , ischemia occurring without symptoms, is a rare possibility that usually need not be considered. Source:http://www.cardiology.org/tools/ecg_abnormalities/STEK.htm

View an ECG Example

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J Point

www.circ.ahajournals.org/cgi/content/full/98/18/1937

The J point in the ECG is the point where the QRS complex joins the ST segment. It represents the approximate end of depolarization and the beginning of repolarization as determined by the surface ECG. There is an overlap of 10 milliseconds. The J point may deviate from the baseline in early repolarization, epicardial or endocardial ischemia or injury, pericarditis, right or left bundle-branch block, right or left ventricular hypertrophy, or digitalis effect. The term J deflection has been used to designate the formation of the wave produced when there is a large, prominent deviation of the J point from the baseline. The J deflection has been called many names, including camel-hump sign, late delta wave, J-point wave, and Osborn wave.

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ECG-AHA 2010

When the patient presents with symptoms and signs of potential ACS, the clinician uses ECG findings (Figure 1, Box 4) to classify the patient into 1 of 3 groups:

1. ST-segment elevation or presumed new LBBB (Box 5) is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men 40 years old); J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old); J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).113

2. Ischemic ST-segment depression >0.5 mm (0.05 mV) or dynamic T-wave inversion with pain or discomfort (Box 9) is classified as UA/NSTEMI. Nonpersistent or transient ST-segment elevation 0.5 mm for <20 minutes is also included in this category. Threshold values for ST-segment depression consistent with ischemia are J-point depression 0.05 mV (-.5 mm) in leads V2 and V3 and -0.1 mV (-1 mm) in all other leads (men and women).113

3. The nondiagnostic ECG with either normal or minimally abnormal (ie, nonspecific ST-segment or T-wave changes, Box 13). This ECG is nondiagnostic and inconclusive for ischemia, requiring further risk stratification. This classification includes patients with normal ECGs and those with ST-segment deviation of <0.5 mm (0.05 mV) or T-wave inversion of 0.2 mV. This category of ECG is termed nondiagnostic.

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Some Clinical Conditions in Which the Electrocardiogram Interpretation Can Be Difficult

Source:Tintinelli 7th

May have ST-segment elevation in the absence of acute myocardial infarction
Early repolarization
Left ventricular hypertrophy
Pericarditis
Myocarditis
Left ventricular aneurysm
Hypertropic cardiomyopathy
Hypothermia
Ventricular paced rhythms
Left bundle-branch block
May have ST-segment depressions in the absence of ischemia
Hypokalemia
Digoxin effect
Cor pulmonale and right heart strain
Early repolarization
Left ventricular hypertrophy
Ventricular-paced rhythms
Left bundle-branch block
May have T-wave inversions in the absence of ischemia
Persistent juvenile pattern
Stokes-Adams syncope or seizures
Post-tachycardia T-wave inversion
Postpacemaker T-wave inversion
Intracranial pathology (central nervous system hemorrhage)
Mitral valve prolapse
Pericarditis
Primary or secondary myocardial diseases
Pulmonary embolism or cor pulmonale from other causes
Spontaneous pneumothorax
Myocardial contusion
Left ventricular hypertrophy
Ventricular-paced rhythms
Left bundle-branch block
Right bundle-branch block

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