Journal of Veterinary Emergency and Critical Care 00(0) 2016, pp 16

doi: 10.1111/vec.12454

Case report

Severe hyperkalemia presenting with

wide-complex tachycardia in a puppy with
acute kidney injury secondary to leptospirosis
Jean V. Rubanick, DVM, DACVECC; Ryan C. Fries, DVM, DACVIM; Carly E. Waugh, DVM,
DACVIM and Medora B. Pashmakova, DVM, DACVECC

Abstract

Objective To describe a case of hyperkalemia coinciding with wide-complex tachycardia (WCT) in a dog with
acute kidney injury secondary to leptospirosis infection.
Case summary An 11-week-old Golden RetrieverStandard Poodle cross puppy was referred for acute kidney
injury and hepatopathy. WCT coinciding with marked hyperkalemia was identified on presentation. Tachycardia
persisted until resolution of hyperkalemia.
New or unique information provided To our knowledge, this is the first report of severe hyperkalemia
presenting with WCT in a dog. Hyperkalemia should be considered a differential for WCT in dogs.
(J Vet Emerg Crit Care 2016; 00(0): 16) doi: 10.1111/vec.12454
Keywords: arrhythmia, canine, electrolyte imbalance, potassium

Abbreviations

AKI
AV
FAST
MAP
PCR
PD
SA
ST
WCT

acute kidney injury

atrioventricular
focused assessment of sonography in trauma
mean arterial pressure
polymerase chain reaction
peritoneal dialysis
sinoatrial
sinus tachycardia
wide-complex tachycardia

Introduction
Hyperkalemia is traditionally associated with classic
electrocardiogram (ECG) changes and bradycardia. In
addition, persistent, marked hyperkalemia in patients
with kidney failure is a poor prognostic indicator. While
wide-complex tachycardia (WCT) has been reported in
experimentally induced hyperkalemia in dogs,1 this is

From the Department of Small Animal Clinical Sciences, Texas A&M University, College Station, TX 77843.
The authors declare no conflicts of interests.
Address correspondence and reprint requests to
Dr. Rubanick, TAMU 4474, College Station, TX 77843, USA
Email: jrubanick@cvm.tamu.edu
Submitted May 09, 2014; Accepted September 27, 2014.

C Veterinary Emergency and Critical Care Society 2016

the first report describing a case of naturally occurring

hyperkalemia secondary to kidney failure presenting
with WCT in a dog. The WCT (initially presumed to be
ventricular tachycardia) and hyperkalemia were refractory to standard therapies. The WCT converted to sinus
tachycardia (ST) with the administration of calcium gluconate; however, a reduction in sinus rate did not occur
until the resolution of hyperkalemia.

Case Report
An 11-week-old intact male Golden Retriever Standard
Poodle crossbreed, weighing 7 kg, was referred to the
Texas A&M University Small Animal Hospital for acute
kidney injury and hepatopathy. The dog was initially
presented 2 days prior to his primary care veterinarian
for vomiting and diarrhea. Parvovirus testa was negative and the dog was empirically treated with antiemetic
and antiparasitic drugs and subcutaneous fluids. Gastrointestinal signs persisted overnight and the dog was
presented to an emergency hospital the next day for additional fluid therapy. On the third day of clinical signs,
the dog was again presented to his primary care veterinarian for lack of improvement. Serum biochemistry
revealed marked azotemia and increased liver enzyme
activities. The dog was then referred to a tertiary care
facility.
1

J. V. Rubanick et al.

Figure 1: Electrocardiogram (ECG) of a puppy with widecomplex tachycardia and acute kidney injury secondary to leptospirosis. Lead II, paper speed 25 mm/s, 10 mm/mV (a, b), 40
mm/mV (c). (a) ECG trace showing wide-complex tachycardia
seen on presentation associated with severe hyperkalemia. Heart
rate 200/min. No P waves are identified on this trace and there
is a blending of the T wave and QRS complex. (b) ECG trace obtained after calcium gluconate administration. Note the presence
of small positive P waves (arrows) consistent with sinus node activity and atrial depolarization. Heart rate 160/min. (c) ECG trace
demonstrating a normal sinus rhythm obtained after normalization of serum potassium concentration. Heart rate 130/min.

On presentation to the teaching hospital, the dog

was tachycardic (heart rate of 200/min) with weak
femoral pulses, tachypneic, and hypotensive (oscillometric systolic blood pressure of 85 mm Hg). Rectal
temperature was 38C and peripheral capillary oxygen
saturation (SpO2 ) was 90%. Mucous membranes were
icteric. Single-lead ECG revealed a WCT, presumed to be
ventricular in origin (Figure 1a). Lidocaineb 2 mg/kg was
administered IV for initial therapy of hemodynamically
significant ventricular tachycardia. After the initial bolus, the rhythm converted to ST (Figure 1b) for several
minutes. Intravenous access and a blood sample for a venous blood gas and electrolyte analysis were obtained.c
Shortly thereafter, the heart rhythm reverted to a WCT,
which was unresponsive to 2 additional 2 mg/kg IV
doses of lidocaine and initiation of a lidocaine continuous rate infusion at 50 g/kg/min. At this time, the
venous blood gas analysis results were available and revealed marked hyperkalemia (10.94 mmol/L, reference
interval 3.914.4 mmol/L) and azotemia (Table 1).
2

Additional treatments consisted of flow-by O2 supplementation and 2 IV boluses of 200 mL (28.6 mL/kg)
of a balanced electrolyte solutiond to achieve normotension. Albuterole 190 g was administered via aerosol
chamberf to aid redistribution of potassium into the
intracellular space. A calcium gluconateg infusion of
92.9 mg/kg was initiated for cardioprotective effects in
the presence of hyperkalemia. Concurrently, 2 doses of
procainamideh 2 mg/kg each were also administered
IV in an effort to convert the WCT, with no immediate
effect seen. Following calcium gluconate infusion, the
WCT again reverted to ST (heart rate of 160/min) and
this rate and rhythm persisted for the next 36 hours.
Imaging evaluation was performed when patient stability allowed. Thoracic radiographs revealed an alveolar pattern in the right middle and cranial lung lobes and
a mild interstitial pattern in the remaining lung lobes,
suggestive of leptospirosis or uremic pneumonitis. Focused assessment of sonography in trauma ultrasound
exam revealed a subjectively small bladder and peritoneal effusion in all four quadrants (abdominal fluid
score of 4/4).
With the conversion of the heart rhythm to ST and
normalization of mean arterial blood pressure (100
mm Hg), sedation for central venous catheter placement was deemed safe. Buprenorphinei 0.01 mg/kg
and acepromazinej 0.014 mg/kg were administered IV
to facilitate placement of a central venous catheter to
optimize further hemodynamic monitoring and fluid
therapy. Jugular pulses were noted during placement.
An indwelling urinary catheter was also placed and
35 mL of urine was obtained. Samples for CBC (unremarkable), full serum biochemistry with electrolytes
(Table 2), urinalysis (USG 1.010, glucose 14 mmol/L [250
mg/dL]), urine bacterial culture/sensitivity (no growth),
leptospirosis polymerase chain reaction (negative), and
leptospirosis titers (negative) were obtained. Central venous pressures were measured at 11 cm H2 O and continuous ECG showed persistent ST with rates ranging
between 165 and 180/min. A repeat venous blood gas
obtained 3 hours after presentation showed minimal
change in potassium, BUN, and creatinine concentrations (Table 1), at which point an additional crystalloid
bolus of 300 mL, dextrosek continuous rate infusion,
and 0.5 U/kg of regular insulinl were administered IV
to facilitate intracellular potassium translocation. Additional treatments included ampicillinm 28.6 mg/kg IV q
8 h for suspected leptospirosis infection, pantoprazolen
0.14 mg/kg q 24 h IV for mitigation of uremic gastrointestinal ulceration, ondansetrono 0.2 mg/kg IV q
8 h to prevent uremia-induced vomiting and nausea,
buprenorphine 0.01 mg/kg IV q 8 h for abdominal pain,
n-acetylcysteinep 140 mg/kg IV once for its hepatoprotective antioxidant effects, and O2 supplementation via

C Veterinary Emergency and Critical Care Society 2016, doi: 10.1111/vec.12454

Hyperkalemia and wide-complex tachycardia in a dog

Table 1: Venous blood gas analyses during first 4 days of hospitalization in a puppy with wide-complex tachycardia and acute kidney
injury secondary to leptospirosis

Parameter reference interval

2

pH 7.357.50
pCO2
3041 mm Hg
HCO3
2431 mmol/L2
(2431 mEq/L)
Base excess
Blood urea nitrogen
1.077.1 mmol/L
(320 mg/dL)2
Creatinine
18221 mol/L
(0.22.5 mg/dL)
Sodium
142152 mmol/L2
(142152 mEq/L)
Potassium
3.55.0 mmol/L2
(3.55.0 mEq/L)
Chloride
106114 mmol/L2
(106114 mEq/L)
Calcium
1.341.54 mmol/L2
(5.366.16 mg/dL)
Magnesium
0.210.48 mmol/L2
(0.511.17 mg/dL)

0 Presentation

12 hours

24 hours

36 hours

48 hours

72 hours

96 hours

7.268

7.279

7.274

7.363

7.377

7.411

7.45

26.9

28.6

31.1

30.4

29.5

37.6

33.7

12.4
(12.4)
14.8

13.5
(13.5)
13.5

14.5
(14.5)
12.6

17.5
(17.5)
8.2

17.5
(17.5)
7.9

24.1
(24.1)
0.8

23.7
(23.7)
0.6

23
(63)

19
(52)

857
(9.7)

ERR

460
(5.2)

716
(8.1)

371
(4.2)

194
(2.2)

150
(1.7)

141.7
(141.7)

141.1
(141.1)

140.3
(140.3)

138.5
(138.5)

136.6
(136.6)

142.2
(142.2)

144.9
(144.9)

10.94
(10.94)

8.62
(8.62)

7.8
(7.8)

8.15
(8.15)

5.55
(5.55)

4.6
(4,6)

4.09
(4.09)

114.3
(114.3)

111.6
(111.6)

109.8
(109.8)

108.9
(108.9)

105.2
(105.2)

101.4
(101.4)

108.9
(108.9)

1.56
(6.24)

1.59
(6.36)

1.61
(6.44)

1.48
(5.92)

1.5
(6.0)

1.4
(5.6)

1.38

0.85
(2.07)

0.66
(1.61)

0.66
(1.61)

0.74
(1.8)

0.54
(1.31)

0.51
(1.24)

0.47
(1.14)

Too high to read.

cage with inspired oxygen fraction (FiO2 ) of 40% to maintain normoxemia. A synthetic colloidq was administered
overnight to optimize intravascular volume and oncotic
pull. Total urine output was 91 mL (1.14 mL/kg/h), total fluid input was 1.57 L (224 mL/kg), and total body
weight gain was 0.83 kg (12% weight gain) over a 9 hours
30 minutes period. Due to the low urine output despite
aggressive fluid loading, furosemider 0.5 mg/kg IV was
administered and fluid rates were decreased twice by
50% each time. Urine output remained inappropriately
low despite these medical therapies.
Abdominal ultrasonography on the following morning revealed enlarged hyperechoic kidneys and peritoneal and retroperitoneal fluid. A sample of the peritoneal fluid revealed a pure transudate. Potassium and
creatinine concentrations of the fluid (>9 mmol/L and
645 mol/L [7.3 mg/dL], respectively) were nearly identical to that of plasma.
Venous blood gases (q 6 h) continued to show persistent hyperkalemia. Calcium gluconate 71.4 mg/kg
(once), terbutalines 0.011 mg/kg (once), and regular insulin 0.21 U/kg (5 times), were administered throughout day 2 for cardioprotection and continued attempts to


C Veterinary Emergency and Critical Care Society 2016, doi: 10.1111/vec.12454

redistribute potassium intracellularly. During this time,

the ST rate ranged from 154 to 225/min. Additionally,
mannitolt 0.86 g/kg was administered IV to stimulate
urine production, without success. Intravenous fluid administration was discontinued due to volume overload
and persistently low urine output. At that time, the decision was made to evacuate the abdominal effusion
to remove potassium from the body, as well as to initiate peritoneal dialysis once the fluid was evacuated.
Fentanylu 3.6 g/kg and acepromazine 0.01 mg/kg were
administered IV to facilitate percutaneous abdominal
placement of an 8 Fr pigtail catheterv . The catheter was
placed cranially and to the left of the prepuce using ultrasound guidance and aseptic technique. A total of 573 mL
(81.9 mL/kg) of effusion was drained by gravity flow at
the time of catheter placement. Peritoneal dialysis was
then performed using techniques described elsewhere3,4
with dialysate consisting of 4.5% dextrose and 1000
U/L unfractionated heparinw in a balanced electrolyte
solution.x Dialysate dextrose composition was adjusted
based on the patients hydration status. Body weight and
venous blood gases were obtained every second dialysis
cycle. A total of 7 cycles were performed in 12 hours.

J. V. Rubanick et al.

Table 2: Serum biochemistries during days 1 and 4 of hospitalization and day 12 after presentation (8 days after discharge) in a
puppy with wide-complex tachycardia and acute kidney injury
secondary to leptospirosis

Parameter reference interval

Phosphorus
0.942.0 mmol/L
(2.96.2 mg/dL)
Glucose
3.37.5 mmol/L
(60135 mg/dL)
Lactate
1.095.19 mmol/L
(9.946.8 mg/dL)
Cholesterol
3.116.4 mmol/L
(120247 mg/dL)
Blood urea nitrogen
1.810.4 mmol/L
(529 mg/dL)
Creatinine
26.5177 mmol/L
(0.32 mg/dL)
Magnesium
0.70.86 mmol/L
(1.72.1 mg/dL)
Calcium
2.332.95 mmol/L
(9.311.8 mg/dL)
Total protein
5778 g/L
(5.77.8 g/dL)
Albumin
2436 g/L
(2.43.6 g/dL)
Globulin
1738 g/L
(1.73.8 g/dL)
Alanine aminotransferase
10130 U/L
(10130 units/L)
Alkaline phosphatase
24147 U/L
(24147 units/L)
Gamma-glutamyl transferase
025 U/L
(025 units/L)
Total bilirubin
014 mol/L
(00.8 mg/dL)
Sodium
139147 mmol/L
(139147 mEq/L)
Potassium
3.34.6 mmol/L
(3.34.6 mEq/L)
Chloride
107116 mmol/L
(107116 mEq/L)

Day 1

Day 4

Day 12

4.36
(13.5)

3.49
(10.8)

2.7
(8.4)

5.1
(92)

5.4
(98)

4.2
(76)

3.05
(27.5)

1.39
(12.5)

NA

5.88
(227)

7.51
(290)

6.88
(265.8)

87.5
(245)

13.6
(38)

8.11
(22.7)

673
(7.61)

199
(2.25)

33.6
(0.38)

1.6
(4)

1.3
(3.1)

NA

3.58
(14.3)

3,18
(12.7)

2.8
(11.2)

47
(4.7)

54
(5.4)

49
(4.9)

21
(2.1)

24
(2.4)

30
(3)

25
(2.5)

30
(3)

19
(1.9)

293
(293)

187
(187)

37
(37)

689
(689)

468
(468)

176
(176)

13
(13)

11
(11)

3.1
(3.1)

109
(6.4)

43
(2.5)

2.4
(0.14)

142
(142)

148
(148)

142
(142)

9.2
(9.2)

3.9
(3.9)

5.3
(5.3)

106
(106)

97
(97)

107
(107)

Conversion to polyuria occurred during day 2. Thirty

hours after initiation of treatment, urine output was 7.9
mL/kg/h and on day 3 production increased further to
18.630.4 mL/kg/h. Intravenous fluids were restarted
and the rate was adjusted to match urine output. Serum
potassium concentration began to decrease after 6 dialysis cycles (day 3) and was within reference limits at 72
hours of hospitalization. Significant polyuria was noted
over the next 4 days, requiring IV fluid rates of up to 57
ml/kg/h to match output. Coinciding with the polyuria
and decrease in potassium concentration, the dogs heart
rate normalized (100128/min; Figure 1C). Polyuria continued until day 8 of hospitalization before gradual resolution. With the significant improvement in clinical status and the dogs kidney values, he was discharged from
the hospital on day 9 with a 14-day course of doxycycline 7.14 mg/kg PO q 12 h. Convalescent titers obtained
7 weeks from initial presentation showed titers of 1:800
for both Leptospira grippotyphosa and L. icterohemorrhagiae. Follow-up serum biochemistry obtained 3 months
following discharge was normal.

Discussion
Hyperkalemia can result in a variety of conduction disturbances within the heart. Arrhythmias such as sinus
arrest, asystole, sinoventricular rhythm, sinus bradycardia, atrioventricular block, and WCT have all been
described.59 Classic ECG findings include tall, peaked
T waves progressing to prolongation of the P-R interval,
decreased P wave amplitude, eventual atrial standstill,
widening of the QRS complex, ventricular fibrillation,
and asystole.1012
The difference between the resting and threshold potentials determines the excitability of a tissue. The potassium concentration gradient is the primary determinant
of the resting membrane potential7,9,12,13 such that when
serum potassium concentration increases, the transmembrane gradient decreases. This results in a less negative
resting membrane potential and leads to a slower rate
of rise of phase 0 of the action potential and slower
conduction.9 This decrease in the conduction velocity creates the widened QRS complex on the surface
ECG.1,9,14 Hyperkalemia is a known cause of WCT in
human patients5,7 and tachycardia with concurrent severe hyperkalemia has been recognized in cats.6,8,15 To
the authors knowledge, this is the first report of severe
hyperkalemia presenting with WCT in a dog.
WCT may be ventricular or supraventricular in origin. While narrow, upright QRS complexes are almost
always supraventricular in origin, wide QRS complexes
may originate from within the ventricles or above the


C Veterinary Emergency and Critical Care Society 2016, doi: 10.1111/vec.12454

Hyperkalemia and wide-complex tachycardia in a dog

ventricles. It has been shown that 80% of WCTs in

people are ventricular in origin.16 Supraventricular
tachycardias with aberrant ventricular conduction or
bundle branch block will result in monomorphic, WCT
with no obvious P waves and this can be easily confused
with ventricular tachycardia.1,17
Metabolic derangements and electrolyte abnormalities, of which this patient had many, may result in
aberrant ventricular activation.1,9,10,12,17 This patient presented with a WCT and no identifiable P waves on the
ECG. The lack of P waves in this case is most likely
the result of atrial standstill secondary to severe hyperkalemia. Other causes for a lack of P waves include atrial
fibrillation, which would produce an irregularly irregular rhythm, and atrial standstill due to cardiomyopathy.
These causes are not likely given the regularity of the
underlying WCT and return of sinus activity (P waves)
after treatment with calcium gluconate and resolution of
the hyperkalemia (Figure 1B). Confirming the origin of
the WCT as ventricular tachycardia or supraventricular
associated with hyperkalemia is impossible without an
electrophysiological study. However, there are several
characteristics of the canine conduction system that support a wide-complex supraventricular tachycardia as the
most likely interpretation of the initial ECG in this case.
First, while the atria are more sensitive to hyperkalemia than the ventricles,1,10 the sinoatrial (SA) node
is less sensitive than the surrounding atria and can continue to stimulate the ventricles in the absence of atrial
activity, so-called sinoventricular conduction.18 During
this rhythm the heartbeat originates in the SA node as
usual, crosses the atria through the internodal tracts (but
the impulse does not spread outward to activate the atrial
myocardium, thus, no P wave), and then passes through
the atrioventricular node and His-Purkinje system in the
usual sequence. The ECG appearance is a regular rhythm
with widened QRS complexes and no P waves.19 This remains the case until SA activity ceases at higher serum
potassium concentration.
Second, intracardiac electrode recordings from the
hearts of experimentally induced hyperkalemic dogs
have shown that the bundle of His is the least sensitive portion of the conduction system to the depressant effects of hyperkalemia.1 In these studies, wide
QRS complexes with no visible P waves on the surface ECG were preceded by His bundle potentials on
intracardiac electrograms, signifying a supraventricular
pacemaker for these complexes.1,10 Additionally, it was
shown that hyperkalemia decreases the rate of firing of
the primary pacemakers, while accelerating subsidiary
pacemakers.20 This may explain, in part, why the junctional rate was faster than normal. While the His bundle may have been initiating the cardiac impulses, hyperkalemia delayed conduction through the ventricular

C Veterinary Emergency and Critical Care Society 2016, doi: 10.1111/vec.12454

myocardium, resulting in a widened QRS complex on

the surface ECG.1,913
Lastly, while it has been shown experimentally that
hyperkalemia-induced ventricular arrhythmias occur,
they typically immediately precede asystole.1,9,10 Furthermore, the ventricular-type of escape rhythm seen
with hyperkalemia is associated with a very low rate. If
not corrected immediately this rhythm quickly devolves
to cardiac arrest (eg, ventricular fibrillation or pulseless
electrical activity) within minutes. The arrhythmia in this
case did not respond appropriately to sodium-channel
blocking drugs and, while some supraventricular tachyarrhythmias do respond to procainamide administration, this lends strong supportive evidence to a diagnosis of wide-complex supraventricular tachycardia rather
than VT. Persistent depolarization of the resting membrane potential, as is the case with hyperkalemia, inactivates sodium channels.7,14 Atrial and ventricular myocytes rely on sodium for depolarization12 and, in theory,
administering a sodium-channel blocker in the presence
of hyperkalemia should have potentiated its effect. In
fact, case reports in human medicine have demonstrated
that sodium-channel blocker administration in the face
of hyperkalemia-induced ventricular arrhythmias can
result in asystole and death as a result of potentiation.5
Of interest in this case is the fact that the dog remained tachycardic until normokalemia was restored.
In a study looking at ECG abnormalities in naturally occurring hyperkalemic dogs and cats, there was no correlation between potassium concentration and heart rate.8
The same study showed that ECG findings not previously reported in association with hyperkalemia were
seen in 30% of the population. The final reversion to an ST
in this patient coincided with administration of calcium
gluconate, which supports the theory that hyperkalemia
contributed to the WCT seen on presentation. However,
the sinus rate remained increased until hyperkalemia,
pain, acidosis, azotemia, and volume status were all normalized suggesting that these other comorbidities were
contributing to the persistent tachycardia.
This report highlights the findings of a previous
study,21 which reported that 45% of dogs would have
been misdiagnosed without a convalescent leptospirosis
titer. Antimicrobial therapy for leptospirosis in the face
of negative urine and blood polymerase chain reactions
were likely lifesaving in this patient. Supportive evidence for treatment in this case included the presence of
liver enzyme increases and respiratory changes, which
are previously described comorbidities.21,22 In a recent
study identifying atypical features of leptospirosis,21
43% of dogs were found to have radiographic evidence
of pulmonary disease. Respiratory difficulty was only
reported in 2% of the population in the same study.
Radiographic evidence of pulmonary disease and liver
5

J. V. Rubanick et al.

involvement alone were also identified. Identification of

some of the less commonly seen features of leptospirosis
highlights the importance of obtaining convalescent
titers. Seven weeks after presentation the dog in this
case had an increased convalescent titer, confirming the
initial diagnosis.

Conclusion
This report details the atypical presentation of marked
hyperkalemia in a dog with kidney failure secondary to
leptospirosis infection. While WCT in association with
hyperkalemia in cats and people are well recognized,
there are no reports of this occurrence in dogs. Hyperkalemia should be considered a differential for WCT in
dogs and should prompt immediate electrolyte analysis,
with treatment targeted at rapid correction of the electrolyte abnormality.

Footnotes
a
b
c
d
e
f
g
h
i
j
k
l
m
n
o
p
q
r
s
t
u
v
w
x

IDEXX Laboratories, Westbrook, MN.

Hospira, Lake Forest, IL.
Stat Profile, NOVA Biomedical Corporation, Waltham, MA.
Normosol-R, Hospira.
GlaxoSmithKline, Research Triangle Park, NC.
AeroKat Feline Aerosol Chamber, Trudell Medical International, London,
ON.
APP Pharmaceuticals, Schaumburg, IL.
Hospira.
Reckitt Benckiser, Richmond, VA.
Vedco, Inc, St. Joseph, MO.
Hospira.
Lilly, Indianapolis, IN.
APP Pharmaceuticals.
Pfizer, Philadelphia, PA.
GlaxoSmithKline.
Hospira.
Hespan, B. Braun Medical Inc, Bethlehem, PA.
Intervet/Merck Animal Health, Summit, NJ.
APP Pharmaceuticals.
Neogen Corporation, Lexington, KY.
Baxter International Inc, Deerfield, IL.
Infiniti Medical, Menlo Park, CA.
APP Pharmaceuticals, Schaumburg, IL.
Lactated Ringers solution, Hospira.

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C Veterinary Emergency and Critical Care Society 2016, doi: 10.1111/vec.12454