Page 213 - Feline Cardiology
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218 Section F: Arrhythmias and Other Electrocardiographic Abnormalities
QRS
II
P
T
T
Figure 18.3. Sinus tachycardia in an anxious cat with compensated hypertrophic cardiomyopathy. Heart rate = 210 beats/minute.
25 mm/sec, 2 cm = 1 mV.
weaker, or stronger intensity than normal depending on diagnostic test of choice, and it is generally performed
diastolic filling time, presence or absence of structural if a patient’s heart rate seems inappropriately high given
heart disease, and intravascular volume status, among the patient’s context; if the rate remains elevated in a
Arrhythmias stress-associated sinus tachycardia, or pallor in anemia despite calm environment and no identifiable illness); if
other factors.
sustained manner (>60 seconds at >240 beats/minute
Other findings, such as an anxious demeanor with
the rhythm is irregular; or if overt clinical signs sugges-
cases, are often apparent to varying degrees on the extra-
cardiac physical examination. A heart murmur may tive of syncope are observed, since none of these features
is consistent with sinus tachycardia.
sometimes be heard only when a cat’s heart rate is ele- Importantly, treatment of sinus tachycardia should
vated. Since heart rate and inotropy (force of ventricular consist of correcting its inciting causes, not treating the
contractility) are both increased by sympathetic stimu- arrhythmia. Suppression of sinus tachycardia itself, such
lation, the clinician’s impression may be that a cat’s as with a beta-blocker or calcium-channel blocker, may
increased heart rate is responsible for the generation of prove to be catastrophic when the rhythm was a natural
the murmur, when in fact the increased systolic force is compensatory response (reflex tachycardia) providing a
more likely causative. Importantly, this phenomenon necessary increase in cardiac output in a systemically ill
may be harmless, as in many cases of dynamic midright patient.
ventricular obstruction (Rishniw and Thomas 2002), or
may be indicative of structural heart disease, as in the Sinus Bradycardia
obstructive form of hypertrophic cardiomyopathy. A cat A rhythm that is sinus in origin but that occurs at a rate
with a murmur audible only when provoked or aroused lower than that of NSR (<110 bpm) is termed sinus bra-
is 6.1 times more likely to have dynamic ventricular dycardia (Figure 18.4). Sinus bradycardia is a rhythm
outflow tract obstruction than a cat that does not that virtually always occurs as a consequence of an extra-
develop a murmur under the same circumstances (Paige cardiac influence, generally one that increases vagal
et al. 2009). Therefore, the presence of a heart murmur tone. Examples include spontaneous factors (e.g., sleep),
noted only during sinus tachycardia is neither diagnostic medical effects (e.g., opiate drugs), and systemic disor-
of heart disease nor reassuring of its absence, and when ders such as hypoglycemia (Little 2005). Subjectively,
a murmur is noted only when a cat’s heart rate is high, cats commonly develop sinus bradycardia in shock syn-
investigation of cardiac structure, beginning with echo- dromes such as severe hypovolemia (Boothe et al. 1985)
cardiography, is warranted. or septic peritonitis (16% of cases) (Costello et al. 2004).
Sinus tachycardia is the most common cause of an Interestingly, in cats experimentally made hypovolemic
elevated heart rate in overtly healthy cats in a clinical through massive phlebotomy (bled 25 ml/kg), the heart
setting. ECGs performed on 27 normal cats identified rate decreases, and replacement with equal or larger
rhythms of sinus origin at a mean heart rate of 182 ± 20 volumes of lactated Ringer’s solution causes an increase
beats/minute (Hamlin 1989), indicating that more than in heart rate—the opposite sequence of events expected
half of healthy cats have sinus tachycardia when from baroreceptor reflex predominance, as in dogs
restrained for the purpose of ECG evaluation. (Costello et al. 2004). This phenomenon is well-
Differential diagnoses include atrial tachycardias, recognized in feline practice; the mechanisms remain to
ventricular tachycardia, and rarely atrioventricular be clarified, but potential explanations include SA nodal
reciprocating tachycardias (macroreentry such as the hypoperfusion, rapid downregulation or disturbance
Wolff-Parkinson-White syndrome). The ECG is the of catecholamine receptors, cervical/thoracic trauma