Changes in the mean electrical axis may occur if the anatomical position of the heart is altered or if the relative mass of the right and left ventricles is abnormal, as it is in certain cardiovascular disturbances. For example, the axis tends to shift toward the left (more horizontal) in short, stocky individuals and toward the right (more vertical) in tall, thin persons. Additionally, in left or right ventricular hypertrophy (increased myocardial mass of either ventricle), the axis shifts toward the hypertrophied side.

Cardiac arrhythmias are disruptions in either impulse initiation or impulse propagation. Impulse initiation disturbances include those that originate from the SA node and various ectopic foci. The primary disruptions in impulse propagation are reentrant rhythms and conduction blocks.

Mechanisms that alter the firing frequency of cardiac pacemaker cells were previously described. Changes in the firing rate of the SA node are typically caused by cardiac autonomic nerves. When the firing rate of the SA node decreases, the heart rate also decreases (bradycardia). Conversely, increased SA node firing results in an elevated heart rate (tachycardia). Examples of electrocardiograms (ECGs) of sinus tachycardia and sinus bradycardia are depicted in Figure 16.29. The P, QRS, and T deflections are all normal, but the duration of the cardiac cycle (the PP interval) is altered. The changes in cardiac frequency are usually gradual. A rhythmic variation of the PP interval at the respiratory frequency, known as respiratory sinus arrhythmia, is a common and normal occurrence.

Various physiological, pharmacological, and pathological processes can hinder the transmission of an impulse through the AV node. The site of blockage can be more precisely localized by an electrocardiogram of the His bundle, as shown in Figure 16.30. To obtain such tracings, an electrode catheter is inserted into a peripheral vein and advanced centrally into the right side of the heart until the electrode lies in the AV junctional region. When the electrode is correctly positioned, a distinct deflection (H in Figure 16.30) is recorded as the cardiac impulse passes through the bundle of His. The time intervals required for propagation from the atrium to the bundle of His and from the bundle of His to the ventricles (His-to-ventricle interval) can be accurately measured. Abnormal prolongation of the atrium-to-His or His-to-ventricle interval indicates blockage above or below the bundle of His, respectively.

Premature depolarizations occasionally occur in most normal individuals, but they are more common in certain abnormal conditions. These depolarizations may originate in the atria, AV junction, or ventricles. One type of premature depolarization follows a normally conducted depolarization at a constant time interval (the coupling interval). If the normal depolarization is somehow suppressed (e.g., by vagal stimulation), the premature depolarization is also eliminated. These premature depolarizations are referred to as coupled extrasystoles, or simply extrasystoles.

Figure 16.30 displays an electrocardiogram of the His bundle (lower tracing, retouched) and a lead II recording of the scalar electrocardiogram (upper tracing). The deflection H, which represents conduction of the impulse over the bundle of His, is clearly visible between the atrial and ventricular (V) deflections. The conduction time from the atria to the bundle of His is denoted by the A-H interval, and that from the bundle of His to the ventricles is denoted by the H-V interval.
Changesinthemeanelectricalaxismayoccuriftheanatomicalpositionoftheheartisalteredoriftherelativemassoftherightandleftventriclesisabnormal,asitisincertaincardiovasculardisturbances.Forexample,theaxistendstoshifttowardtheleft(morehorizontal)inshort,stockyindividualsandtowardtheright(morevertical)intall,thinpersons.Inaddition,inleftorrightventricularhypertrophy(increasedmyocardialmassofeitherventricle),theaxisshiftstowardthehypertrophiedside.
Cardiac arrhythmias are disturbances in either impulse initiation or impulse propagation. Disturbances in impulse initiation include those that arise from the SA node and •Fig. 16.29 Electrocardiographic Tracings of Heart Rhythms. A, Normalsinusrhythm.B, Sinus tachycardia.C, Sinusbradycardia.
those that originate from various ectopic foci. The principal disturbances in impulse propagation are reentrant rhythms and conduction blocks.
Mechanisms that vary the firing frequency of cardiac pacemaker cells were described previously. Changes in the firing rate of the SA node are usually produced by cardiac autonomic nerves. When the firing rate of the SA node is decreased, the heart rate also decreases (bradycardia). Conversely, increased SA node firing results in elevation of the heart rate (tachycardia). Examples of ECGs of sinus tachycardia and sinus bradycardia are shown in
Fig. 16.29 . The P, QRS, and T deflections are all normal, but duration of the cardiac cycle (the PP interval) is altered. The changes in cardiac frequency are characteristically gradual. A rhythmic variation of the PP interval at the respiratory frequency (i.e., a respiratory sinus arrhythmia) is a normal, common occurrence (see
Fig. 18.7
Various physiological, pharmacological, and pathological processes can impede transmission of an impulse through the AV node. The site of block can be localized more precisely by an electrocardiogram of the His bundle (Fig.
16.30 ). To obtain such tracings, an electrode catheter is inserted into a peripheral vein and advanced centrally into the right side of the heart until the electrode lies in the AV junctional region. When the electrode is properly positioned, a distinct deflection (H in
Fig. 16.30 ) is registered as the cardiac impulse passes through the bundle of His. The time intervals required for propagation from the atrium to the bundle of His and from the bundle of His to the ventricles (His-to-ventricle interval) may be measured accurately. Abnormal prolongation of the atrium-to-His or His-to-ventricle interval indicates block above or below the bundle of His, respectively.
Premature depolarizations occur occasionally in most normal individuals, but they arise more commonly in certain abnormal conditions. Such depolarizations may originate in the atria, AV junction, or ventricles. One type of premature depolarization follows a normally conducted depolarization at a constant time interval (the coupling interval). If the normal depolarization is suppressed in some way (e.g., by vagal stimulation), the premature depolarization is also abolished. Such premature depolarizations are called coupled extrasystoles, or simply extrasystoles, and they
P A H V T QRS 0.2 sec •Fig. 16.30 ElectrocardiogramoftheHisbundle(lower tracing, retouched)andleadIIrecordingofthescalarelectrocardiogram(upper tracing). ThedeflectionH,whichrepresentsconductionoftheimpulseoverthebundleofHis,isclearlyvisiblebetweentheatrial andtheventricular(V)deflections.TheconductiontimefromtheatriatothebundleofHisisdenotedbytheA-Hinterval;thatfromthebundleofHistotheventricles,bytheH-Vinterval.(CourtesyofDr.
J.
Edelstein.)