Chapter 6 Flashcards

1
Q

What are some indications for MI? (Think about H&P, Cardiac Enzymes, and the ECG)

A

H&P: prolonged, crushing substernal chest pain radiating to the jaw, shoulders, or left arm, associated with nausea, diaphoresis, and SOB; high risk co-morbidity: DM, elderly, HLD

Cardiac Enzymes: Elevated creatine kinase (CK), particularly MB isoenzyme (do not rise until 6hr after MI, return to normal within 48hrs); Elevated Troponin, more sensitive (within 2~3hrs, and stay elevated for sevral days)

ECG: During an acute MI, ECG evolves through 3 stages (T peaking followed by T inversion; ST elevation; Appearance of Q waves)

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2
Q

Is T wave inversion always diagnostic of MI?

A

No. T wave inversion by itself is indicative only of ischemia, and many things can cause T wave inversion, such as bundle branch block and ventricular hypertrophy with repolarization abnormalities.

Yet T wave inversion of MI are Symmetrical, whereas most other ones are Asymmetric, with a gentle downslope and a rapid upslope.

(A) The symmetric T wave inversion in a patient with ischemia. (B) An example of asymmetric T wave inversion in a patient with left ventricular hypertrophy and repolarization abnormalities.

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3
Q

What’s “pseudonormalization”?

A

Patient who already has inversed T waves, experiencing new episodes of ischemia, which may cause the inversed T to revert to normal. Recognition requires comparing the current to previous tracing

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4
Q

Be familiar with how ST elevation looks like, don’t confuse with J point elevation

A

Two examples of ST segment elevation during an acute infarction: (A) Without T wave inversion and (B) with T wave inversion.

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5
Q

Should we concern about J point elevation?

A

Not really. The J point represents the end of depolarization and beginning of repolarization of the ventricle. J point elevation is a very common phenomenon in young, health individuals. The ST segment usually returns to baseline with exercise. Has no pathologic implications whatsoever. With myocardial injury, the ST segment has a distinctive bowing upwards and awkward joining with the T wave, whereas with J point elevation, the T wave maintains its independent waveform. J-point is the point at which the QRS complex meets the ST wave.

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6
Q

What does ST elevation signify? Which one is more concerning, concave upward or downward?

A

ST elevation sigifies myocardial injury. Usually return to baseline within a few hours. Persistent ST elevation indicates formation of a ventricular aneurysm. ST segment elevation with an upward convexity is usually benign, especially when seen in healthy, asymptomatic individuals.ST segment elevation with a downward concavity is more likely to be due to acute coronary syndrome.

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7
Q

What does appearance of new Q waves indicate, and what’s the criteria for significant Q waves?

A

Irreversible myocardial cell death. It is diagnostic of MI.

Criteria:

Q>0.04sec; Depth must be at least 1/3 of the R wave

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8
Q

Are the following Q waves significant?

A

The Q waves in leads I and aVF are significant. The Q wave in lead V2 is too shallow and narrow to qualify (don’t confuse the tiny Q wave with the large S wave). The Q wave in lead aVR is immense, but Q waves in aVR are never significant!

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9
Q

Know the main coronary arteries, and the four basic anatomic sites of myocardial infarction.

A
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10
Q

Know the location each infarction area covers, which artery is occluded and the associated leads.

A

Inferior: diaphragmatic surface of the heart. Often caused by occlusion of right coronary artery or its desending branch. ECG changes can be seen in II, III, and aVF, the inferior leads

Lateral: the left lateral wall. Often due to occlusion of the left circumflex artery. Changes occur in I, aVL, V5, and V6, the left lateral leads

Anterior: anterior surface of left ventricle. Usually caused by occlusion of left anterior descending artery. Changes seen in V1-V6

Posterior: posterior surface of the heart. Occlusion of the right coronary artery. There are no leads overlay the posterior wall, thus we have to look for reciprocal changes in the anterior leads, especially V1

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11
Q

What’s “reciprocal changes”?

A

Leads located some distance from the infarction site will see an increase of electrical forces, tall R waves. These changes are called reciprocal changes. It applies to not only Q waves but also ST and T changes.

Reciprocal changes in an inferior infarction. The acute ST elevation and T wave peaking in lead II is echoed by the ST depression and T wave inversion in lead V3.

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12
Q

Identify the location of the infarction

A

A fully evolved inferior infarction. Deep Q waves can be seen in leads II, III, and aVF.

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13
Q

Identify the location of the infarction

A

An acute lateral wall infarction. ST elevation can be seen in leads I, aVL, V5, and V6. Note also the deep Q waves in leads II, III, and aVF, signifying a previous inferior infarction. Notice the deep Q waves in leads V3 through V6. These are the result of probably another previous anterior infarction, which affects the anterior wall of the left ventricle

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14
Q

Identify the location of the infarction

A

An anterior infarction with poor R wave progression across the precordium.

Anterior infarction is not always associated with Q wave formation. In some pts, there may be only a loss of the normal pattern of precordial R wave progression. In normal hearts, the amplitude of R waves should increase at least 1mV per lead as you go from V1 to V5.

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15
Q

Identify the location of the infarction

A

A posterior infarction. In lead V1, the R wave is larger than the S wave. There is also ST depression and T wave inversion in leads V1 and V2.

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16
Q

Where is the infarct? Is it acute?

A

This is an example of an evolving anterior infarction. There is ST segment elevation in leads V2 and V3 as well as poor R wave progression.

17
Q

Where is the infarct? Is it acute?

A

This tracing shows an acute posterior and inferior infarction (most posterior infarctions are accompanied by evidence of inferior infarction). ST segment elevation with peaked T waves can be seen in leads II, III, and aVF, indicating an acute inferior infarction. There is also evidence of posterior wall involvement, with a tall R wave, ST segment depression, and T wave inversion in lead V1.

18
Q

What’s the anatomic difference between a transmural infarction and a subendocardial infarction?

A
19
Q

How will the ECG look like when pt experiences an angina attack?

A

Three examples of the EKG changes that can accompany angina: (A) T wave inversion; (B) ST segment depression; and (C) ST segment depression with T wave inversion (the ST segment and T waves merge seamlessly).

20
Q

How do you differentiate the ST depression of angina from that of non-Q wave infarction?

A

W/ angina, ST usually return to baseline shortly after the attack has subsided. Non-Q wave infarction, ST remain down for at least 48hrs, and the cardiac enzymes will be elevated.

21
Q

When will you have angina w/ ST elevation?

A

Prinzmetal’s angina, with ST segment elevation.

22
Q

Causes for ST elevation/depression

A

Elevation: evolving transmural infarction, Prinzmetal’s angina, J point elevation, Apical ballooning syndrome, Acute pericarditis, Acute myocarditis, Hyperkalemia, Pulmonary embolism, Brugada syndrome, Hypothermia.

Depression: typical angina, Non-Q wave infarction,Hypokalemia, digitalis effect

23
Q

What type of ST depression should we concern about?

A

(A) Downsloping ST depression. (B) Upsloping ST depression. (C) Horizontal ST depression. Only A and C are highly suggestive of coronary artery disease.