Page 200 - Clinical Small Animal Internal Medicine

168 Section 3 Cardiovascular Disease

impulse to conduct from the sinus node through the node (see Figures 17.10 and 17.12). Finally, ventricular
VetBooks.ir atria and the AV node and bundle of His. Conduction in hypertrophy can increase the amplitude and duration of
the QRS complex (albeit to a lesser degree than a bundle
the AV node is markedly slower, allowing time between
the mechanical contraction of the atria and the ventri-
the case of right heart enlargement).
cles. On the surface ECG, this conduction delay pro- branch block) or change the mean electrical axis (as in
duces a short isoelectric segment following the P‐wave,
contributing to the PR interval. The normal PR interval
in dogs and cats is shown in Table 17.3. Increased dura- The T‐wave
tion of the PR interval indicates abnormally slow con- Following the QRS complex is another short, relatively
duction in the AV node, called first‐degree AV block. isoelectric segment, the ST segment, followed by the T‐
Intrinsic AV node disease as well as certain drugs, if wave, representing the ventricular repolarization. The
overdosed (beta‐blockers or Ca channel blockers), may ST segment connects the QRS complex and the T‐wave
result in first degree AV block. Varying PR intervals are (see Figure 17.3). However, since it is usually difficult to
noted in cases of sinus arrhythmia or certain forms of determine exactly where the ST segment ends and the
second‐degree AV block. Abnormally short PR intervals T‐wave begins, the relationship between the QT interval
are rare and encountered in instances of accessory path- and T‐wave should be examined together. In general, the
way‐mediated arrhythmias. ST segment should not be either elevated or depressed
compared to baseline by more than 0.2 mV. In dogs and
The QRS Complex cats, ST segment abnormalities are occasionally detected
in cases of myocardial disease (dilated cardiomyopathy),
When the electrical impulse emerges from the AV node, congenital heart disease (subaortic stenosis), electrolyte
it enters the ventricles rapidly via the bundle of His, the imbalances, acute hypoxia (anesthesia) or suspected
right and left bundle branches and Purkinje network, myocardial infarction (rare).
producing the QRS complex on the surface ECG. The The T‐wave represents ventricular repolarization. The
QRS complex thus represents ventricular depolariza- normal T‐wave in both dogs and cats demonstrates a
tion. Standard nomenclature describes the first negative high degree of variability and can be positive, negative,
deflection as the Q‐wave, the first positive deflection as biphasic, or of very low amplitude; however, the T‐wave
the R‐wave, and the first negative deflection following should be consistent from beat to beat during normal
the first positive deflection as the S‐wave (see Figure 17.3). rhythm. The normal characteristics of the T‐wave in
Note that normal QRS complexes do not necessarily dogs and cats are shown in Table 17.3. Compared to
contain all three waveforms, and in dogs, a high degree human patients, T‐wave changes in the dog and cat are
of individual variability is seen. The normal sequence of relatively nonspecific and poorly characterized. T‐wave
ventricular depolarization results in a QRS complex of abnormalities can be seen in instances of electrolyte
relatively short duration and with a net positive polarity abnormalities, hypoxia, conduction abnormalities, or
in leads II, III, and aVF. The normal duration and ampli- drug toxicity (i.e., digoxin).
tude of the QRS complex in the dog and cat are shown in The QT interval is a measure of the time between the
Table 17.3. start of the Q‐wave (or R‐wave if there is no Q) and the
A key component of ECG analysis is inspection of the end of the T‐wave and represents the entire depolariza-
QRS morphology in lead II, which can provide clues to tion and repolarization of the left and right ventricles. If
the beat’s origin, its conduction through the ventricle, abnormally prolonged or shortened, there is a risk of
and the potential presence of ventricular hypertrophy. developing ventricular arrhythmias. Prolongation of the
QRS complexes generated by a beat of supraventricular QT interval may be due to an adverse drug reaction (i.e.,
origin (sinus node or supraventricular foci such as the quinidine toxicity). Some antiarrhythmic drugs, like
atria or AV nodal junction) are typically narrow and pos- amiodarone or sotalol, work by creating a pharmacologic
itive in lead II, while those that originate from ventricu- QT prolongation. A shortened QT can be associated
lar foci are wider (increased duration) and “bizarre” in with hypercalcemia (Box 17.1).
their appearance compared to normal sinus beats.
Conduction disturbances within the ventricles can also
alter the morphology of the QRS complexes. For instance,
the presence of a right or left bundle branch block slows Evaluation of the ECG
conduction through the ventricular tissue in the respec-
tive side. This results in a QRS complex of longer dura- Important features of the ECG that require analysis
tion (wide) despite the fact that the beat may have include heart rate, rhythm, mean electrical axis (MEA),
originated from a supraventricular focus or the sinus waveform morphology, and criteria for heart enlarge-