Page 106 - Small Animal Internal Medicine, 6th Edition

78 PART I Cardiovascular System Disorders

recognized, however, that even with apparently complete signs of cardiac disease present (e.g., heart murmur,
conversion to sinus rhythm, the risk of sudden death from cardiomegaly)? Are there additional abnormalities (e.g.,
VetBooks.ir a lethal arrhythmia may remain. It is also important to fever, abnormal blood chemistry or hemogram values,
respiratory compromise with hypoxia, other extracardiac
remember that all antiarrhythmic drugs can have adverse
effects, including provoking additional arrhythmias (proar-
medications? Correct what can be corrected!
rhythmic effect). disease, trauma, or pain)? Is the animal receiving any
Various arrhythmias and their electrocardiographic char- 3. Decide whether to use antiarrhythmic drug therapy. Con-
acteristics are described in Chapter 2. This section provides a sider signalment, history, clinical signs, and underlying
general approach to managing cardiac rhythm disturbances. disease, as well as the potential benefits/risks of the
Nevertheless, much remains to be learned about effective drug(s) under consideration.
arrhythmia management and the prevention of sudden 4. If an antiarrhythmic drug is to be used, define the goals
death. of therapy for this patient.
5. Initiate treatment and determine drug effectiveness.
1. Record and interpret an electrocardiogram (ECG) (Box Adjust dose or try alternate agents, if needed.
4.1); identify and define any arrhythmia. An extended 6. Monitor patient status. Assess arrhythmia control (con-
ECG recording period may be necessary (e.g., Holter or sider repeated Holter monitoring), manage underlying
event monitoring or extended in-hospital monitoring). disease(s), and watch for adverse drug effects and other
2. Evaluate the whole patient, including history, physical complications.
examination findings, and clinical/laboratory test results.
Are signs of hemodynamic impairment evident (e.g.,
episodic weakness, syncope, signs of CHF)? Are other DIAGNOSIS AND MANAGEMENT OF
COMMON ARRHYTHMIAS

BOX 4.1 Cardiac arrhythmias in a given animal often occur inconsis-
tently and are influenced by drug therapy, prevailing auto-
ECG Interpretation Guide nomic tone, baroreceptor reflexes, and variations in heart
rate. Treatment decisions are based on consideration of the
1. Determine the heart rate. Is it too fast, too slow, or origin (supraventricular or ventricular), timing (premature
normal? or escape), and severity of the rhythm disturbance, as well
2. Is the rhythm regular or irregular?
3. Is sinus rhythm present (with or without other as the clinical context. Accurate ECG interpretation is
abnormalities), or are there no consistent P-QRS-T important. Although a routine (resting) ECG documents
relationships? arrhythmias present during the recording period, it provides
4. Are all P waves followed by a QRS and all QRS only a glimpse of the cardiac rhythm occurring over time.
complexes preceded by a P wave? Because marked variation in frequency and severity of
5. If premature (early) complexes are present, do they arrhythmias can occur over time, potentially critical arrhyth-
look the same as sinus QRS complexes (implying mias are easy to miss. For this reason, Holter (or other ambu-
atrial or junctional [supraventricular] origin), or are latory ECG) monitoring can be useful in assessing the
they wide and of different configuration than sinus severity and frequency of arrhythmias and monitoring treat-
complexes (implying a ventricular origin [or possibly ment efficacy. Some rhythm abnormalities do not require
abnormal ventricular conduction of a supraventricular therapy, whereas others demand immediate aggressive treat-
complex])?
6. Are premature QRS complexes preceded by an ment. Close patient monitoring is especially important in
abnormal P wave (suggesting atrial origin)? patients with more serious arrhythmias.
7. Are there baseline undulations instead of clear and Supraventricular tachyarrhythmias occur from various
consistent P waves, with a rapid, irregular QRS mechanisms, including reentry involving the AV node,
occurrence (compatible with atrial fibrillation)? accessory pathways, or sinoatrial (SA) node, as well as
8. Are there long pauses in the underlying rhythm abnormal automaticity within atrial or junctional tissue.
before an abnormal complex occurs (escape beat)? Many patients have atrial enlargement. Common underlying
9. Is an intermittent AV conduction disturbance present? heart diseases include chronic mitral or tricuspid valve
10. Is there a lack of consistent temporal relationship degeneration with regurgitation, DCM, congenital malfor-
between P waves and QRS complexes, with a slow mations, and cardiac neoplasia. Other factors also may pre-
and regular QRS occurrence (implying complete AV dispose to atrial tachyarrhythmias (Box 4.2).
block with escape rhythm)?
11. For sinus and supraventricular complexes, is the VPCs occur with disorders that affect cardiac tissue
mean electrical axis normal? directly or indirectly through neurohormonal effects (see
12. Are all measurements and waveform durations within Box 4.2). For instance, disorders of the central nervous
normal limits? system (CNS) can produce abnormal autonomic neural
effects in the heart, and provoke ventricular or supraven-
See Chapter 2 for more specific information. tricular arrhythmias (brain-heart syndrome). When VPCs