Abnormal Q waves

1. Normally QRS complex is .04-.12 seconds total in duration. Various configurations of the QRS complex may occur and the term AQRS complex@ is used to describe this complex of ventricular depolarization, regardless of the deflections present, however the Q-wave is not the dominant deflection of the complex.

(8-19, 8-17) 2. Under abnormal conditions, a Apathological Q-wave@ may be present. Characteristics of the Apathological Q-wave@ are Q-wave duration is $ .04 sec (one small square) and amplitude is $ 1/3 of the total QRS complex.

Three Degrees of Myocardial Damage

1. Ischemia

a. Physiology

1. Represents hypoxemic tissue

2. Initial phase of the infarction process.

3. Usually begins in the endocardium and advances toward the epicardium.

4. Becomes the outermost area of a completed MI.

b. Prognosis

1. Salvageable if treated aggressively and promptly.

c. Treatment

1. Reperfuse the area.

2. Decrease the oxygen demand.

d. Signs and symptoms

1. Ischemic area is site of irritability and is electically unstable-PVC=s.

2. Chest (or refered) discomfort or pressure (Angina Pectoris)

e. ECG changes

1. T-wave inversion

-Most common

-Inverted T-wave is symmetrical.

-Usually very first ECG change.

2. ST-segment depression (Possible)

-AJ-point@ is below the baseline

-Flat, horizontal ST-segment

-Present in positive stress tests.

2. Injury

a. Physiology

1. Represents severe hypoxemia.

2. Develops as time progresses if ischemia goes without intervention. (Injured tissue is surrounded by ischemic tissue.)

3. Cell membrane becomes unstable.

4. Spreads from endocardium to epicardium.

5. Becomes middle zone in a completed MI.

b. Prognosis

1. Potentially salvageable if oxygen can be delivered to the cells. Very aggressive treatment is needed to save tissue.

c. Treatment

1. Pain management/oxygenation

2. Hemodynamic manipulation

3. Intracoronary thrombolysis

4. Emergency Procedure (i.e. PTCA, Myocardial Revascularization).

d Signs and Symptoms

1. Injured site is also a site of irritability-PVC=s

2. Chest (or refered) discomfort or pressure

3. Enzymes changes can be present

4. ST-segment elevation may be seen without enzyme elevations.

e. ECG changes

1. ST-segment

-Elevated during acute injury process

2. T-wave inversion (Subendocardial), Possible Hyperacute T=s during acute injury (Transmural)

-Some ischemia may be continuing.

-If ST-segment is very elevated, T-wave may be pulled up and over the baseline, therefore T-wave may not be seen.

3. Infarct

a. Physiology

1. Represents necrotic tissue which may be through all (transmural) or partial (subendocardial) muscle layers.

2. Endpoint of infarction process.

3. Cell membranes rupture.

4. Spreads endocardium to epicardium

5. Surrounded by zones of injured and ischemic tissue (loose boundaries.)

6. Becomes central core of completed MI.

b. Prognosis

1. Irreversible

2. Necrotic tissue is replaced with scar tissue.

c. Treatment

1. Limit extension of MI, by treating injured and ischemic tissue. (Oxygen, nitroglycerin, Ca-Channel Blockers, Vasodilators, Beta-Blockers, Thrombolysis, PTCA, CABG)

2. Assistance during recovery process.

d. Signs and symptoms

1. Electrically stable

2. Dead tissue cannot initiate or transmit an impulse, therefore no PVC=s or chest (or refered) discomfort or pressure.

e. ECG changes

1. Pathological Q-wave

2. Usually indicative of a transmural MI.

3. Some of the ECG changes described for ischemia and injury may also be present as different areas may have different damage processes occurring simultaneously.

1. Acute Phase

(8-6, 8-8) a. Initial minutes to first hours

b. Extreme ST-segment elevation

c. QRS may be difficult to see

d. Tall hyperacute T-wave (current of injury = damage to epicardial layer)

2. Evolving Phase

(8-7) a. Begins within first hours to first days of onset.

b. ECG changes present dependent upon level of damage:

1. Inverted T-wave - ischemia symmetrical

2. Development of pathological Q-wave B infarct

3. Resolving Phase

a. Occurs within weeks of onset

b. ECG changes:

1. Q-wave remains permanently on ECG.

2. AAcute@ changes resolve

-T-waves WNL

-ST-segment WNL

1. Mirror image of the involved wall

(8-4, 8-5) a. Seen in wall of LV opposite from site of MI.

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Acute MI Reciprocal Change

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Anterior Wall Inferior Wall

Lateral Wall Inferior Wall

Inferior Wall Anterior a/o Lateral Wall

 

 

b. Reciprocal ECG changes

1. Tall R-wave opposite of a Q-wave

2. ST-segment depression is opposite elevation.

3. Positive T-wave is opposite of inverted T-wave.

4. Timeframe for reciprocal changes

a. Seen only in acute phase (gone by evolving and resolving phase.)

b Occurs within minutes to the first day of MI onset.

2 Differentiating characteristics between MI and reciprocal change on ECG

a. Note the ST-segment depression seen with ischemia

1. Indicator of ischemia if this is the only ECG change on the 12-lead ECG.

2. Indicator of reciprocal change if changes related to an acute MI are seen elsewhere on the 12-lead ECG.

(8-9, 8-10, 8-11) 1. Anterior Wall Infarct - loss of R-wave progression in precordial leads, QS in V3, V4

2. Anteroseptal Wall Infarct - QS in V1 & V2, septum supplied by LAD coronary artery

3. Anterolateral Wall Infarct - QS in V5, V6, possibly aVL & lead I, left circumflex coronary artery

(8-12, 8-13, 8-14) 4. Inferior Wall Infarct - Significant Q=s in II, III, aVF, usually RCA

(8-15) 5. Posterior Wall Infarct - Tall R=s & ST Depression in V1& V2. If V6 involved = posterior-lateral, If II, III, aVF involved = infero-posterior

(9-1) 1) ST-Depression

(9-2)

Angina Pectoris

(9-3) 1) Symptoms of CAD

(9-4) - dull burning pain left arm, neck, back, substernal pressure (9-5) precipitated by exertion, stress, cold ...

2) Silent Ischemia

- ST-depression with no signs of Angina Pectoris

(9-8) 3) Prinzmetals Angina

- Transient transmural ST-elevation typically during rest or sleep.

- etiology - coronary artery vasospasm causing transmural ischemia.

Exercise Testing

1) > 1mm horizontal or downsloping ST-segment is abnormal (positive test)

2) 1mm ST-segment depression of only the J-point with rapid upsloping ST-segment is normal during exercise.

3) Normal Exercise Test does not exclude CAD

- 10% false positives due to:

- digitalis, hypokalemia, LVH, BBB, WPW syndrome

- false negatives also occur

1) Persistent ST-depression - Is not transient as observed in subendocardial ischemia

- Generally no Q-waves occur

- Subendocardial MI effects ventricular repolarization (ST-T) and not ventricular depolarization (QRS)

(9-6) 2) T-wave inversion

(9-7)

(9-9) Differential Diagnosis - must take all leads into account

ST Elevation ST-Depression

-Acute transmural MI -Subendocardial ischemia

-Prinzmetals Angina (transient) -LVH with strain

-Ventricular Aneurysm -Reciprocal depression in acute - Acute Pericarditis transmural injury Acurrent of injury@

- Normal variant in young adult - Digitalis

- V1, V2, of LVH or LBBB - Hypokalemia

- Evolving phase of Q-wave MI

- Normal in aVR, V1 in adults

- Juvenile T-wave inversion pattern V1-V3

- Right ventricular strain pattern

- Evolving phase of percarditis

- RBBB in right precordials

- LBBB in left precordials

1) Mechanical 2) Electrical

- heart failure - arrhythmias

- LV aneurysm - conduction disturbances

- Rupture of heart - V-tach

- pericarditis - V-fib

- embolism

- expansion of MI

1. Diagnosis of damage (transmural vs. subendocardial or ischemia vs. injury vs. infarction) is done by ECG, enzymes, patient history and diagnostic tests.

2. ECG changes to look for include T-wave inversion, ST-segment elevation or depression, presence or absence of pathological Q-waves.

3. All phase (ischemia, injury, infarction) and stages (acute, evolving, resolving) can be seen if contact is made soon enough.

4. Reciprocal changes occur in acute stages primarily, possibly observed in early evolving phase.