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Premature ventricular contraction or ventricular extrasystoles is due to the contraction of the ventricles initiated by the Purkinje fibers instead of the SAN. It is otherwise normal, but sometimes it indicates decreased oxygenation of the myocardium. This is since the ventricles are contracting prior to maximal filling with blood, so less oxygen is carried around. It is perceived as palpitations or skipped beat. It requires no pharmacological treatment in most people. It looks like the following on the ECG:

150 ECG Problems

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Page 1: 150 ECG Problems

Premature ventricular contraction or ventricular extrasystoles is due to the contraction of the ventricles initiated by the Purkinje fibers instead of the SAN.

It is otherwise normal, but sometimes it indicates decreased oxygenation of the myocardium. This is since the ventricles are contracting prior to maximal filling with blood, so less oxygen is

carried around. It is perceived as palpitations or skipped beat. It requires no pharmacological treatment in most people. It looks like the following on the ECG:

Digoxin is usually prescribed for patients with atrial fibrillation.

Page 2: 150 ECG Problems

It has specific effect on the ECG but note that digoxin effect is not the same as digoxin toxicity.

Some of the main features will be:o Downward sloping ST segments in leads V5-6o Flattened, inverted or biphasic T waves

Biphasic is the most common T wave abnormality where there is an initial negative and a terminal positive deflection.

It is usually seen in leads with prominent R waves e.g. V4-6. The 1st negative part will be continuous with depressed ST segment. The terminal part can be peaked or have a prominent U wave superimposed

on it. o Shortened QT-interval i.e. <0.38s

Other possible features will be:o Prominent U waves, especially in leads V2-3o Mild PR interval prolongation of up to 240ms (increased vagal tone)o Peaking of terminal portion of T waveso J point depression

Digoxin is usually given to AF patients, so in any AF patient, look for digoxin’s effects.

The QT interval represents the time taken for ventricular depolarization and repolarization.

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It is the time taken from start of QRS complex to end of ST segment. The usual length is from 0.38-0.42s. The length is inversely proportional to the heart rate.

o Longer the QT interval, lower the heart rate.o Shorter the QT interval, higher the heart rate.

However, QT interval varies with body mass and heart rate, so it is corrected to give the QTc. The QTc is derived using the Bazett formula if heart rate is 60-100.

o QTc = QT/(R-R interval)0.5

At heart rates above 100, the Framingham correction are used instead. QTc is prolonged if >440ms in men and >460ms in women. QTc longer than 500ms is a risk factor for Torsades des Pointes. Causes of long QT interval:

o Hypothermiao MIo Hypocalcemiao Hypokalemiao Hypomangesiaemia o Raised ICPo Congenital long QT syndromeo Drugs: anti-depressants, anti-histamines, macrolides, anti-psychotics and

antiarrhythmics (fleicanide, amiodarone, procainamide) Conversely, QT is shortened if QTc is <350ms. Causes of short QT interval include:

o Hypercalcemiao Congenital short QT syndromeo Digoxin

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