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3/24/26

 


Pressure over load Volume over load

Like in hypertension, ischemic heart disease (IHD)

LV strain pattern—ST depression with T inversion in V5, V6, L1,

and aVL leads

Like in mitral or aortic regurgitation

Shows prominent Q waves, positive T waves in V5, V6,

L1, and aVL

Step 7: Look for Evidence of Infarction/St Segment Abnormalities

ST Segment

ST segment is isoelectric and at the same level as subsequent PR-interval

The length between the end of the S wave (end of ventricular depolarization) and the beginning of

repolarization

From J point on the end of QRS complex, to inclination of T wave.

Causes of ST segment elevation

Ischemia

Early repolarization

Acute pericarditis: ST elevation in all leads except aVR

Pulmonary embolism

Hypothermia

Hypertrophic cardiomyopathy

High potassium

Cerebrovascular accident

Acute sympathetic stress

Brugada syndrome

Cardiac aneurysm

Left ventricular hypertrophy

Idioventricular rhythm including paced rhythm.

Causes of ST segment depression

Myocardial ischemia/non-ST-elevation myocardial infarction (NSTEMI)

Reciprocal change in STEMI

Posterior MI

Digoxin effect (reverse tick mark/“sagging” morphology, resembling Salvador Dali’s moustache)

Hypokalemia

Bundle branch block

Ventricular hypertrophy

Ventricular pacing.

ECG CHANGES IN MYOCARDIAL INFARCTION (MI)

There are two types of MI. ST segment elevation myocardial infarction (STEMI) and non-STEMI

(NSTEMI). ST elevation myocardial infarction criteria:

ST elevation in >2 chest leads >2 mm elevation

ST elevation in >2 limb leads >1 mm elevation

Q wave >0.04 s (1 small square).

Location of MI Lead with ST changes Affected coronary artery

Anterior V1, V2, V3, V4 Left anterior descending (LAD) artery

Septum V1, V2 LAD

Left Lateral I, aVL, V5, V6 Left circumflex

Inferior II, III, aVF Right coronary artery (RCA)

Right atrium aVR, V1 RCA

Posterior Posterior chest leads RCA

Right ventricle Right sided leads RCA

Ischemia Injury Infarct

T-wave inversion (flipped T)

ST segment depression

T wave flattening

Biphasic T waves

ST segment elevation of greater than 1 mm in at

least 2 contiguous leads

Heightened or peaked T waves

Directly related to portions of myocardium

rendered electrically inactive

Significant Q wave where none

previously existed

Why?

Impulse traveling away from the

positive lead

Necrotic tissue is electrically dead

Sequential ECG changes in STEMI

0 hour Pronounced/hyperacute Tall T wave initially ST elevation (convex type)

1–24

hours

Depressed R wave, and pronounced T wave. Pathological Q waves may appear within hours or may take greater than 24 hours indicating full-thickness MI. Q wave is pathological if it is wider

than 40 ms or deeper than a third of the height of the entire QRS complex

Days Exaggeration of T wave continues for 24 hours

1–2

Days

later

T wave inverts as the ST elevation begins to resolve. Persistent ST elevation is rare except in the

presence of a ventricular aneurysm

Weeks

later

ECG returns to normal T wave, but retains pronounced Q wave

Non-ST-Elevation MI

Non-ST-elevation MI is also known as subendocardial or non-Q-wave MI.

In a PT with acute coronary syndrome (ACS) in which the ECG does not show ST elevation,

NSTEMI (subendocardial MI) is suspected if

ST depression (A)

T wave inversion with or without ST depression (B)

Q wave and ST elevation will never happen

A ST depression is more suggestive of myocardial ischemia than infarction.

ELECTROLYTES AND ECG

Hypocalcemia: Prolonged ST segment and QT intervals.

Hypercalcemia

Shortened ST segment

Widened T wave and short QT

Hypokalemia

ST depression

Shallow, flat, and inverted T wave

Prominent U wave and P waves.

Hyperkalemia

Tall, peaked T waves

Flat P waves

Widened QRS complex

Prolonged PR interval

Sine wave.

Fig. 11.8: ECG changes in seen with potassium.

Hypomagnesemia

Tall T waves

Depressed ST segment.

Hypermagnesemia

Prolonged PR interval

Widened QRS complexes.

EXAMPLES

Example 1

12-lead ECG showing

Rate 110 bpm

Rhythm Sinus rhythm

Axis Normal

P wave Duration 0.08 sec and normal morphology

PR interval/segment 0.12 sec

PR segment elevation in aVR

QRS 0.08 sec

ST segment Elevation in V2-V6, I, aVL

Depression in aVR

T wave Normal

QT interval 0.32 sec

Final diagnosis Acute pericarditis

Example 2

12-lead ECG showing

Rate 85 bpm

Rhythm Sinus

Axis Normal

P wave Duration 0.12 sec and normal morphology

PR interval/segment 0.16 sec

QRS 0.08 sec

ST segment Elevation in II, III, aVF (elevation in Lead III > II)

Depression in V1-V6, I, aVL

T wave Corresponds to ST–T changes.

QT interval 0.36 sec

Final diagnosis Inferior wall MI with signs of RV infarction

Example 3

12-lead ECG showing

Rate 200 bpm

Rhythm Regular

Axis Normal

P wave Retrograde

PR interval/segment

QRS 0.08 sec (narrow complex)

ST segment Normal

T wave Normal

QT interval 0.28 sec

Final diagnosis Supraventricular tachycardia-atrioventricular nodal reentry tachycardia (SVT-AVNRT)

Example 4

12-lead ECG showing

Rate 75 bpm

Rhythm Junctional

Axis Normal

P wave Absent

PR interval/segment –

QRS 0.14 sec notching at J point (V2)

ST segment Minimal elevation in V3-V5

No reciprocal changes

T wave Tall T steeple waves in precordial leads, concordant with QRS

QT interval 0.36 sec

Final diagnosis Hyperkalemia

Example 5

12-lead ECG showing

Rate Atrial—80 bpm; Ventricular—50 bpm

Rhythm Junctional escape

Axis Normal

P wave Present

PR interval/segment –

QRS 0.08 sec independent of P waves

ST segment Normal

T wave Normal

QT interval 0.36 sec

Final diagnosis Complete heart block

Example 6

12-lead ECG showing

Rate 70 bpm (6 sec rule)

Rhythm Irregular

Axis Normal

P wave Absent, presence of fibrillary waves

PR interval/segment –

QRS 0.08 sec varying RR interval

ST segment Normal

T wave Normal

QT interval 0.32 sec

Final diagnosis Atrial fibrillation

Example 7

12-lead ECG showing

Rate 250 bpm

Rhythm Regular

Axis Left-northwest

P wave AV dissociation

PR interval/segment –

QRS 0.28 sec (Broad complex)

Positive concordance

ST segment –

T wave -

QT interval -

Final diagnosis Monomorphic ventricular tachycardia (VT)

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A Systematic Approach to Chest X-rays

C H A P T E R

12

RADIOLOGY

We shall discuss practical aspects of radiology under following sections:

Approach to chest X-rays

Approach to CT scans

Approach to MRI scans

Contrast agents

APPROACH TO CHEST X-RAYS

Reading into the Chest Radiograph

The 10 Step Program

What type of view

Exposure/penetration

Inspiratory versus expiratory film

Rotation

Angulation

Soft tissues and bony structures

Trachea

Hilum/mediastinum

Diaphragm

Lung fields

Cardia

Type of View

Chest X-ray

PA view

AP view

Lateral view

PA view (posteroanterior view) (Fig. 12.1)

The ray of beam is from posteroanteriorly with the film in front of the patient.

AP view (anteroposterior view) (Fig. 12.2)

The ray of beam is from anteroposteriorly with the film behind the patient.

3.

Fig. 12.1: Posteroanterior view.

Fig. 12.2: Anteroposterior view.

Lateral view (Fig. 12.3)

The ray of beam is from one side with the film placed on the opposite side of the patient.

Fig. 12.3: Lateral view.

Differences between PA view and AP view of chest X-ray

PA view (Fig. 12.4) AP view (Fig. 12.5)

Fundic gas shadow Usually present Absent

Clavicles Seen over the lung fields and more

horizontal

Seen above the apex of lung field and more oblique

Scapula Inner borders are away form the lung

fields

Inner borders are seen over the lung

fields

Ribs Posterior ribs are better seen and more oblique

Anterior ribs are better seen

Apparent cardiomegaly Not seen Seen

Spine Better seen Not seen

The distance between the projector and

the patient

6 feet 40 inches

Fig. 12.4: PA view. Fig. 12.5: AP view.

Exposure/Penetration

Penetration is the degree to which X-ray passes through the body. Figure 12.6 depicts the grading of

shadow in X-ray film.

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