Normal electrocardiogram

• P-Q or P-R Interval• The time between the beginning of the P wave

and the beginning of the QRS complex is the interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles=0.16 second

• Q-T Interval • Contraction of the ventricle lasts almost from

the beginning of the Q wave (or R wave, if the Q wave is absent) to the end of the T wave. This interval is called the Q-T interval and ordinarily is about 0.35 second.

Rate of Heartbeat as Determined from the Electrocardiogram

• 60/ QRS-QRS interval(0.83)=72

Monophasic action potential from a ventricular muscle fiber during normal cardiac function, showing rapid depolarization and then repolarization occurring slowly during the plateau stage but rapidly toward the end. Below, Electrocardiogram recorded simultaneously.

Recording the depolarization wave (A and B) and the repolarization wave (C and D) from a cardiac muscle fiber.

Instantaneous potentials develop on the surface of a cardiac muscle mass that has been depolarized in its center.

Flow of current in the chest around partially depolarized ventricles.

Conventional arrangement of electrodes for recording the standard electrocardiographic leads. Einthoven's triangle is superimposed on the chest.

Normal electrocardiograms recorded from the three standard electrocardiographic leads

Einthoven’s lawII = III + I

Chest Leads (Precordial Leads)Connections of the body with the electrocardiograph for recording chest leads. LA, left arm; RA, right arm.

Augmented Unipolor Limb Leads

two of the limbs are connected through electrical resistances to the negative terminal of the electrocardiograph, and the third limb is connected to the positive terminal. When the positive terminal is on the right arm, the lead is known as the aVR lead; when on the left arm, the aVL lead; and when on the left leg, the aVF lead.

Mean vector through the partially depolarized ventricles

Axes of the three bipolar and three unipolar leads.

Vectors drawn to represent potentials for several different hearts, and the "axis" of the potential (expressed in degrees)

for each heart.

Determination of a projected vector B along the axis of lead I when vector A represents the instantaneous potential in the

ventricles.

Determination of the projected vector B along the axis of lead I when vector A represents the instantaneous potential in the ventricles.

Determination of projected vectors in leads I, II, and III when vector A represents the instantaneous potential in the

ventricles.

Shaded areas of the ventricles are depolarized (-); nonshaded areas are still polarized (+). The ventricular vectors and QRS complexes 0.01 second after onset of ventricular depolarization (A); 0.02 second after onset of depolarization (B); 0.035 second after onset of depolarization (C); 0.05 second after onset of depolarization (D); and after depolarization of the ventricles is complete,

0.06 second after onset (E)

Generation of the T wave during repolarization of the ventricles, showing also vectorial analysis of the first stage of repolarization. The total time from the

beginning of the T wave to its end is approximately 0.15 second.

Depolarization of the atria and generation of the P wave, showing the maximum vector through the atria and the resultant vectors in the three

standard leads. At the right are the atrial P and T waves. SA, sinoatrial node.

QRS and T vectorcardiograms.

Plotting the mean electrical axis of the ventricles from two electrocardiographic leads (leads I and III).

Left axis deviation in a hypertensive heart (hypertrophic left ventricle). Note the slightly prolonged QRS complex as well.

High-voltage electrocardiogram in congenital pulmonary valve stenosis with right ventricular hypertrophy. Intense right axis

deviation and a slightly prolonged QRS complex also are seen.

Left axis deviation caused by left bundle branch block. Note also the greatly prolonged QRS complex

Right axis deviation caused by right bundle branch block. Note also the greatly prolonged QRS complex

Low-voltage electrocardiogram following local damage throughout the ventricles caused by previous myocardial

infarction.

Effect of a current of injury on the electrocardiogram.

J point as the zero reference potential of the electrocardiograms for leads I and II. Also, the method for

plotting the axis of the injury potential is shown by the lowermost panel.

Current of injury in acute anterior wall infarction. Note the intense injury potential in lead V2.

Injury potential in acute posterior wall, apical infarction.

Recovery of the myocardium after moderate posterior wall infarction, demonstrating disappearance of the injury potential

that is present on the first day after the infarction and still slightly present at 1 week.

T disorders:

1- Block in Purkinje

2- Ischemia with short depolarization period in base of heart

3- Digital toxicity

Left axis deviation caused by left bundle branch block. Note also the greatly prolonged QRS complex

Ischemia in base of heart

Digital toxicity

Sinus tachycardia (lead I).

Sinus bradycardia (lead III).

Sinoatrial nodal block, with A-V nodal rhythm during the block period (lead III).

Prolonged P-R interval caused by first degree A-V heart block (lead II).

Second degree A-V block, showing occasional failure of the ventricles to receive the excitatory signals (lead

V3).

Complete A-V block (lead II).

Premature Contractions

Causes of ectopic foci are (1) local areas of ischemia; (2) small calcified plaques at different points in the heart, which press against the adjacent cardiac muscle so that some of the fibers are irritated; and (3) toxic irritation of the A-V node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine

Atrial premature beat (lead I).

A-V nodal premature contraction (lead III).

PVC

1- prolonged ORS2- high voltage QRS3-Inverse T

Paroxysmal Tachycardia

Ventricular paroxysmal tachycardia (lead III).

Circus movement, showing annihilation of the impulse in the short pathway and continued propagation of the impulse in the

long pathway.

(1) A long pathway typically occurs in dilated hearts. (2)

Decreased rate of conduction frequently results from (a)

blockage of the Purkinje system, (b) ischemia of the muscle,

(c) high blood potassium levels, or (d) many other factors. (3)

A shortened refractory period commonly occurs in response

to various drugs, such as epinephrine, or after repetitive

electrical stimulation

Fibrillation in a heart

Ventricular fibrillation (lead II).

Application of electrical current to the chest to stop ventricular fibrillation.

Atrial fibrillation (lead I). The waves that can be seen are ventricular QRS and T waves.

Pathways of impulses in atrial flutter and atrial fibrillation.

Atrial flutter-2:1 and 3:1 atrial to ventricle rhythm (lead I).

Abnormal left axis deviation

Anterior heart MI