other disturbances (electrolyte, hypothermia, drugs, other heart diseases)

Question 1

hyperkalemia

Answer 1

Book:

• > Tall tented T waves (should not be confused with acute MI, since they are rather diffused rather than focused on a region which might indicate a local MI)
• > With increased potassium in blood, PR interval becomes prolonged, and P wave disappears after a while.
• > Ultimately, the QRS widends untill it meres with the T wave, forming a sine wave pattern.
• • Might develop to Ventricular fibrillation

Potassium is vital for regulating the normal electrical activity of the heart.
Increased extracellular potassium reduces myocardial excitability, with depression of both pacemaking and conducting tissues.
Progressively worsening hyperkalaemia leads to suppression of impulse generation by the SA node and reduced conduction by the AV node and His-Purkinje system, resulting in bradycardia and conduction blocks and ultimately cardiac arrest.

Question 2

Hypokalemia

Answer 2

• > ST segment depression
• > Flattening of the T wave with prolongation of the QT interval.
• > Apperance of the U wave.

Decreased extracellular potassium causes myocardial hyperexcitability with the potential to develop re-entrant arrhythmias

Question 3

Hypocalcemia

Answer 3

Longer QT interval

**Torsades de pointes may occur, but is much less common than with hypokalaemia or hypomagnesaemia.

Question 4

Hypercalcemia

Answer 4

-> The main ECG abnormality seen with hypercalcaemia is shortening of the QT interval

In severe hypercalcaemia, Osborn waves (J waves) may be seen

Question 5

Hypothermia

Answer 5

• > Everything slows down. Sinus bradycardia is common and all the segments and intervals become prolonged.
• > A virtually diagnostic type of ST elveation may be seen. It consists of an abrupt ascent right at the J point and then an equally sudden plunge back to the baseline. The resultant configuration is called a J wave or Osborn wave.
• > Various arrhytmias may appear- Slow atrial fibrillation

Question 6

Drugs- Digitalis-

Answer 6

ST-T wave changes- so called Digitalis effect:

• > Downsloping ST depression with a characteristic “sagging” appearance (see below).
• > Flattened, inverted, or biphasic T waves.
• > Shortened QT interval.

Toxic levels of Digitalis-

• > SA node supression
• > Conduction block (Any of the levels are seen)
• > Tachyarrhythmias

Question 7

Pericarditis (not sure if relevent)

Answer 7

Often confused with MI since the similar apperance.

Life on fast lane:

• > Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).
• > Reciprocal ST depression and PR elevation in lead aVR (± V1).
• > Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.
• > Pericardial effusion dampens the electrical output of the heart, resulting in low voltage in all leads.

** May also see electrical alternans (vector changes for all the waves in each beat since the heart “swims in fluid”)

Patients complaints also differ in pericarditis- Pain is usually sharp, exacerbated by inspirations and coughing and felt in the entire anterior chest wall.

Question 8

Myocarditis (Not sure how important)

Answer 8

Many things appear.

Sinus tachycardia.
QRS / QT prolongation.
Diffuse T wave inversion.
Ventricular arrhythmias.
AV conduction defects.
With inflammation of the adjacent pericardium, ECG features of pericarditis can also been seen (= myopericarditis).