Page 241 - Feline Cardiology

246 Section F: Arrhythmias and Other Electrocardiographic Abnormalities

surviving despite life-threatening serum potassium provided they are able to excrete it if excessive (i.e.,
levels and others arresting under seemingly identical or urinary tract is patent and renal function is normal).
less severe conditions. An important observation to Thus, PVCs/VT may be more likely to occur in a hyper-
explain this discrepancy is that graded ECG changes kalemic patient as serum potassium concentrations
reported in the literature are based on infusion of potas- decrease toward normal (Figure 18.24).
sium salts (typically potassium chloride) intravenously Sinus bradycardia may also occur with hyperkalemia
in experimental animals, with simultaneous ECG moni- because hyperkalemia decreases the activity of normal
toring and measurement of serum potassium levels. In pacemaker tissue. Specifically, it decreases the slope of
contrast, feline patients with urethral obstruction, acute phase 4 of diastolic depolarization (Surawicz 1995),
renal failure, reperfusion injury, or any other naturally which slows the heart rate. However, naturally occurring
occurring cause of hyperkalemia, often have one or hyperkalemia also routinely coexists with abnormalities
more concurrent metabolic abnormalities, such as in acid-base status or other serum electrolytes, pain, fear,
hypovolemia, anemia, acid-base disturbances, serum sepsis, and other disorders, all of which may increase
calcium abnormalities, or hyperlactatemia, any of which circulating catecholamine concentrations and cause the
may alter cardiomyocyte membrane potential and opposite—sinus tachycardia. The routine observation
threshold. Therefore, the distinct, step-by-step approach that many cats with even severe hyperkalemia have ele-
Arrhythmias mia are scientifically accurate for experimental studies parameter unreliable for inferring a patient’s serum (K )
vated heart rates makes this physical exam or ECG
to ECG changes associated with progressive hyperkale-
+
(Norman et al. 2006; Tag and Day 2008).
but not absolute in the clinical setting. The presence or
absence of P waves appears to be the most important
Mild to moderate increases in serum potassium (6.6–
hyperkalemia-associated finding in cats, and as noted 7.5 mEq/l) may begin to interfere with cell-to-cell trans-
for atrial standstill (above), more than one ECG lead mission velocity in the ventricles, which explains the
should be evaluated before P waves are considered to be initial QRS complex widening observed in some patients
absent because they may normally be small or inappar- with serum potassium concentrations in this range.
ent in some leads (see Figure 18.23). Moderate to severe hyperkalemia (7.0–8.5 mEq/l) can
Mildly elevated serum potassium levels (5.6– cause PR interval prolongation and absence of P waves
6.5 mEq/l) are associated with greater cell membrane altogether, which are probably the most characteristic
permeability to potassium during repolarization. These ECG findings for hyperkalemia in cats. The atria are
repolarization effects predominate over depolarization more sensitive to hyperkalemia than are the ventricles,
effects. Thus, mild hyperkalemia in cats may be reflected and within the atria, the myocardium is more sensitive
on the ECG as faster ventricular repolarization, i.e., a to the effects of hyperkalemia than are the internodal
shorter than normal QT interval and an abnormally tracts (three sets of specialized fibers in the atria consist-
narrow, often peaked or “tented” T wave (DiBartola and ing of the paired ventral [anterior] pathways, which
Autran de Morais 2006; Surawicz 1995; Ettinger et al. carry electrical activity directly to the AV node, and the
1974). It is a common but serious mistake to think dorsal [posterior] pathway called Bachmann’s bundle,
that tented T waves must always equal hyperkalemia, which is also responsible for left atrial activation). The
because cats may have tall or peaked T waves in health, result when severe hyperkalemia occurs is a sinoven-
and likewise may be mildly or moderately hyperkalemic tricular rhythm, so named because the heartbeat origi-
with minimal or no observable change in T wave mor- nates normally in the SA node, crosses the atria through
phology. Serial ECGs in the same patient, obtained the internodal tracts (but the impulse does not spread
under the same conditions, that show progressively outward—no atrial activation, no P wave), and then
taller T waves are probably the most reliable application passes through the AV node and His-Purkinje system in
of this association; obtunded patients in ICU, or patients the usual sequence. The ECG appearance is a regular
under general anesthesia, are examples where increas- rhythm with normal or slightly widened QRS com-
ingly tall T waves should prompt serum potassium level plexes, and no P waves (Figure 18.25).
measurement. Very high serum potassium concentrations
+
Mild hyperkalemia (e.g., serum K concentration = 6– (>8.5 mEq/l) can be fatal. So many other factors influ-
6.5 mEq/l) may be considered as slightly antiarrhythmic ence the rhythm in these catastrophically ill patients that
because myocardial excitability is reduced compared to an exact cutoff for lethality cannot be established for
normokalemia, without adverse effects on contractility. serum potassium concentration alone. Any cat with a
For this reason, cats with PVCs and/or VT should have serum potassium concentration >8.5 mEq/l is at risk of
serum potassium concentrations that are well within the death from a combination of hyperkalemia and the
normal range and preferably at the upper end of normal, inciting disorder. Experimental studies have shown that