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Chapter 18: Arrhythmias and Other Electrocardiographic Abnormalities 245

was associated with resolution of preexcitation subse- This prolongation of repolarization lengthens the nor-
quently (Rishniw 2000; Riesen and Lombard 2005). mally very brief period of repolarization during which
Structural heart disease was often present concurrently the diastolic membrane potential is near the threshold
(left ventricular concentric hypertrophy/HCM potential. Therefore, hypokalemia-induced prolonga-
[n = 12/24; 50%], restrictive/unclassified cardiomyopa- tion of repolarization opens a window of increased
thy [n = 3/24; 13%], congenital heart disease (unspeci- excitability during which spontaneous ectopic activity
fied) [n = 2/24; 8%], “myocardial disease—other” (such as atrial or ventricular extrasystoles) can occur
[n = 2/24; 8%], dilated cardiomyopathy [n = 1/24; 5%], based on the threshold being reached after the absolute
Ebstein’s malformation of the tricuspid valve plus heart- refractory period by a slowly repolarizing cell. Clinically,
worm disease [n = 1/24; 5%]). In 3/24 cases (13%), the second (arrhythmogenic) effect predominates over
echocardiographic findings were within normal limits. the first (suppressive), and the dominant cardiovascular
The association of preexcitation with Ebstein’s malfor- effect of a serum potassium concentration <3.5 mEq/l in
mation (Meurs and Miller 1993) is intriguing, because cats is an increased risk of spontaneous depolarizations,
this association is well-recognized in the dog and human. notably ventricular extrasystoles (PVCs). Other ECG
Long-term outcome is explicitly described in only 6 manifestations of hypokalemia can include evidence of
cases, and in these cats preexitation seemed to confer a prolonged, abnormal repolarization in the form of U
fair prognosis: 4 cats lived for at least 2–7 months (1 waves (see previous discussion), QT interval prolonga-
with recurrent syncope and then lost to follow-up) and tion, and AV dissociation (Atkins 1991). Because class I Arrhythmias
the remaining 2 were euthanized for other reasons (gas- antiarrhythmics (e.g., lidocaine, mexiletine, quinidine)
trointestinal lymphoma; donation). act on sodium channels that require normal serum
potassium concentrations to function, hypokalemia is
also important as a cause of antiarrhythmic drug refrac-
CARDIAC EFFECTS OF SYSTEMIC POTASSIUM
AND CALCIUM ABNORMALITIES toriness: in a patient whose PVCs are caused by hypo-
kalemia, a decrease in PVC number, or resolution of the
Because cardiac activity depends fundamentally on arrhythmia altogether, is expected with potassium sup-
transmembrane movements of ions, pathologically high plementation alone, whereas treatment with lidocaine
or low systemic concentrations of potassium and calcium during hypokalemia is unlikely to alter the ventricular
may lead to disturbances in cardiac function, some of arrhythmia, but may still cause lidocaine toxicosis if
which can have important effects on the heart’s rhythm. dosing is readministered repeatedly because of pre-
sumed inadequate drug response. This important obser-
Hypokalemia vation has wide-ranging implications in patients with
Serum potassium concentrations are most accurate if dilutional hypokalemia (e.g., trauma patient with large-
measured on blood drawn into lithium heparin (green volume fluid resuscitation) or potassium-wasting meta-
top) tubes. Red top tubes allow coagulation, a process bolic illness (e.g., chronic kidney disease) when PVCs/
that, during platelet activation and aggregation, releases VT occur and the question “When should I treat this
potassium and may artifactually raise the measurement arrhythmia with an antiarrhythmic?” arises. An impor-
by small but clinically significant levels, masking hypo- tant initial step toward answering this question should
kalemia or falsely suggesting hyperkalemia. always be to ensure that normokalemia is present before
A low serum potassium concentration produces two considering antiarrhythmic therapy.
major effects in cardiomyocytes. First, it makes the
resting membrane potential increasingly negative (see Hyperkalemia
Figure 18.13) (DiBartola and Autran de Morais 2006; ECG changes associated with increasing degrees of
Surawicz 1995), which decreases myocyte excitability. hyperkalemia have been clearly categorized and pub-
This effect is a result of the greater difference between lished widely (DiBartola and Autran de Morais 2006;
intracellular and extracellular potassium concentrations Surawicz 1995; Ettinger et al. 1974; Norman et al. 2006).
in hypokalemia compared to normokalemia (hyperpo- According to these criteria, the ECG passes through
larization) and in cardiomyocytes is generally mild and different stages as hyperkalemia becomes more severe,
transient. Second, hypokalemia prolongs repolarization, and accordingly, veterinarians have sought to stratify
increasing action potential duration (DiBartola and the risks associated with hyperkalemia based on ECG
Autran de Morais 2006; Surawicz 1995). Myocyte repo- findings. This stratification has not held up well to clini-
larization depends principally on the activity of potas- cal scrutiny, with some cats having markedly greater
sium currents, notably the delayed rectifiers I Kr and I Ks . serum potassium concentrations than would be expected
With hypokalemia, these currents function more slowly. from the ECG, and others markedly lower, or some cats