What’s Wrong With Murphy? You Make The Call

Help diagnose Murphy the cat.


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Signalment: 4 year old MC domestic short hair cat

History: Murphy has been restless the last few days and has spent a lot of time on the litter box. He has been vocalizing excessively. Today he refused to eat, started vomiting and became progressively more lethargic.

Physical Examination:
T: 97.0  P: 110  R: 14
Murphy is somewhat obese with a BCS of 7/9. He is minimally responsive on presentation. Thoracic auscultation fails to reveal any abnormalities. Abdominal palpation is resented, a large bladder is palpated. Palpation results in obvious discomfort. Pulses are thready. An ECG is obtained.

1. What is the rate and rhythm on this ECG tracing?
2. What are potential differentials for this type of rhythm?
3. What clinical significance does this rhythm have and what other clinical findings could suggest that a severe problem is present?
4. What treatment is recommended for this rhythm?
5. What other diagnostics are appropriate?

1. What is the rate and rhythm on this ECG tracing?

The ECG shows a slow heart rate of approximately 100 BPM. The rhythm does not appear to be sinus, as P-waves cannot be identified. The ventricular complexes are increased in duration and large for a cat ECG.

The T-waves are also quite tall. Based upon the clinical examination findings and because it can be assumed that the cat is blocked, the most likely diagnosis is severe hyperkalemia with apparent sinus arrest in a cat.

With hyperkalemia, a variety of changes can occur, though they are not consistently present. The first changes that classically occur are that the P-wave becomes smaller to the point where it can no longer be seen and the T-wave becomes tall and spiked.

The QRS complex then becomes prolonged in duration. This is because the rising extracellular potassium value raises the resting membrane potential to a point where depolarization of the atrium can no longer occur.

The sinus node and ventricle are more resistant to the effects of elevated potassium concentrations than the atrium. The sinus node will still depolarize and result in the activation of the ventricle without the atrium responding resulting in the absence of a P-wave.

The speed at which cardiac cells depolarize is dependent on how low the resting membrane potential was. In hyperkalemia, the duration of the action potential is prolonged resulting in the prolongation of the QRS complex that is seen. Hyperkalemia also influences repolarization by shortening the time it takes for repolarization to occur resulting in the typical peaked appearance of the T-wave.

2. What are potential differentials for this type of rhythm?

Given the clinical scenario there are few differentials for this rhythm. P-waves can be absent for a variety of reasons. In supraventricular tachycardias (atrial tachycardia, atrial flutter), the P-waves can be buried in the preceding T-wave, making them difficult to identify.

The rhythm in these cases would be very regular and rapid.

Another rhythm to consider would be atrial fibrillation; in this case, however, the rhythm would be markedly irregular. These supraventricular arrhythmias are unlikely in this case given that tachycardia is not present and the QRS is wide, with supraventricular tachycardias the QRS complexes would be narrow.

A ventricular rhythm could be considered as a differential (e.g. ventricular tachycardia). In these cases, however, in most instances a non-conducted P-wave can be identified at times. Rate would also usually be higher.

A rare rhythm disturbance in cats is true sinus standstill. This has previously been identified in cats with dilated cardiomyopathy. Other causes in dogs and humans include myasthenia gravis and some forms of muscular dystrophy.

3. What clinical significance does this rhythm have? What other clinical findings could suggest that a severe problem is present?

Finding the typical changes of hyperkalemia in a cat that has an appropriate clinical history is always of great concern as it indicates in most cases severe and potentially life-threatening severity. Of course having a normal ECG does not rule out dangerously elevated potassium values.

In a study that included both dogs and cats, it was found that only four of 11 animals with a potassium > 10 mmol/L had appropriate ECG changes.1 In another small study it was found that ionized calcium was strongly correlated to a variety of the ECG parameters. Many of the cats had low ionized calcium and all cats with low ionized calcium were hyperkalemic and had “typical” ECG changes. The only cat that was hyperkalemic and normocalcemic had a normal ECG.2

Clinical exam and history can also be suggestive that hyperkalemia may be present. A retrospective study looked at 223 blocked cats.3 A variety of factors were found to be associated with hyperkalemia, which was defined as a potassium concentration above 8.0 mmol/L. Vomiting and anorexia in the history was predictive of hyperkalemia as were decreased body temperature (< 96.6 degrees) and bradycardia (<120).

4. What treatment is recommended for this rhythm?

A variety of treatments have been recommended for hyperkalemia. Some aim to reduce potassium concentrations, while others, such as the administration of intravenous calcium, are considered cardioprotective.

With the severe changes noted on this ECG and the physical exam findings, calcium intravenously (10 percent calcium gluconate, 50-100 mg/kg over 3 to 5 minutes IV with ECG monitoring) would be indicated. This will not decrease potassium concentration, but it does reset the threshold potential.
This re-establishes the usual difference between resting membrane potential and threshold potential, which allows cardiac tissues to become more normally excitable. This effect is short-lived, probably only 30 to 60 minutes.

Once the obstruction is relieved and the kidneys start working again, potassium will of course be excreted. Potassium concentration can, however, be decreased in a variety of ways before unobstructing the cat.

Aggressive fluid therapy is indicated for resuscitation in this cat, and will decrease potassium concentration by dilution. In addition, increasing perfusion will reduce acidosis, which will drive potassium into the cells. Generally physiologic saline is preferred, though other resuscitation fluids can be used.

Use of sodium bicarbonate (1 mEq/kg is a relatively safe empiric dose given slowly i.v.)  is also quite common and also reduces potassium concentration by combating acidosis.

In humans this therapy is no longer recommended and there are some concerns with its efficacy. In addition it would also decrease ionized calcium concentrations.

Insulin is considered a very effective therapy (0.05 to 0.5 U/kg as an i.v. bolus). Insulin stimulates the Na-K ATPase pump to pump potassium into the cell and sodium out. This effect is not dependent upon glucose, however glucose needs to be given to prevent significant hypoglycemia.

In conjunction with the insulin, 1 to 2 grams of dextrose per unit of insulin need to be given. Adding dextrose to the fluids being infused is advisable as the insulin effects will persist for many hours.

5. What other diagnostic tests are appropriate?

Given that it has been previously shown that a variety of acid-base and electrolyte abnormalities occur, it would be ideal to obtain blood gas analysis in this patient. An ionized calcium value would also be of interest since ionized hypocalcemia is common and may contribute to the ECG abnormalities in these more severely affected cats.

Measuring blood pressure would also be ideal in this cat. Blood pressure at presentation has prognostic value.

In a study on blocked cats, normotensive cats (mean arterial blood pressure between 90 and 140 mmHg) had lower body temperature and slower heart rate than cats that were considered hypertensive (>140 mmHg MAP).4  An abnormal cardiac rhythm was detected in 64 percent of the normotensive group but none of the hypertensive group.

The normotensive group also had more severe biochemical changes with 60 percent being azotemic and 55 percent being hyperkalemic, some cats having severe elevations.

In the hypertensive group, fewer were azotemic and the azotemia was much milder than in the normotensive group and only 1 out 8 cats was hyperkalemic. The main concern with this study is that in most  instances a MAP is considered to be markedly hypertensive, most studies have shown MAP to be around 120 in normal cats. 

Depending upon the scenario, additional diagnostics would of course be of interest, including a CBC, chemistry panel, urinalysis and urine culture. These are of less interest in the emergency situation as their determination will have little influence on the initial management of the patient.

1. Tag TL, Day TK. Electrocardiographic assessment of hyperkalemia in dogs and cats. J Vet Emerg and Crit Care 14 supplement 1;S7:2004.
2. Evason M, Carr A, Waldner C. Correlation between serum potassium concentration, serum ionized calcium concentration, serum sodium:potassium ratio and electrocardiographic findings in cats with urethral obstruction. JVIM 18;407:2004.
3. Lee AJ, Drobatz KJ. Historical and physical parameters as predictors of severe hyperkalemia in male cats with urethral obstruction. J Vet Emerg Crit Care 16; 104-111:2006.
4. Malouin A, Milligan JA. Assessment of blood pressure in cats presented with urethral obstruction. J Vet Emerg and Crit Care 14 supplement 1;S3:2004.

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