ECG of the Month

Mandi K. Schmidt Section of Cardiology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126
School of Veterinary Medicine, Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, Philadelphia, PA 19104-6010

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Amara H. Estrada Section of Cardiology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126

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Meg M. Sleeper School of Veterinary Medicine, Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, Philadelphia, PA 19104-6010

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A 3-year-old sexually intact male mixed-breed dog was referred to the University of Florida for evaluation because of emaciation, recumbency, and dull mentation. The dog had a 1-month history of malnutrition with neglect. Results of clinicopathologic analyses performed by the referring veterinarian had indicated that the dog had anemia, hypoglycemia, hypoproteinemia, hypocalcemia, hyponatremia, and hyperphosphatemia. The initial physical examination (day 1) at the University of Florida revealed that the patient was emaciated (body condition score,1 1/9) with extensive muscle atrophy, weakness, and flea infestation. Mucous membranes were white, and capillary refill was undetectable. On auscultation, the dog had an irregular cardiac rhythm with a heart rate of 80 beats/min; no cardiac murmur was ausculted. Diagnostic procedures included a CBC, serum biochemical analyses, assessment of plasma and whole blood taurine concentrations, blood gas analyses, urinalysis, fecal analysis, blood pressure measurement, crossmatching of blood type, thoracic and abdominal radiography, and electro- and echocardiography.

Electrocardiography (performed on day 1) revealed sinus rhythm with ventricular bigeminy and low-voltage QRS complexes. Noninvasive arterial blood pressure measurements revealed hypotension (systolic arterial blood pressure, 60 mm Hg [reference range, 100 to 160 mm Hg]; diastolic arterial blood pressure, 30 mm Hg [reference range, 60 to 100 mm Hg]). Results of the CBC confirmed ongoing anemia (Hct, 14%; reference range, 35% to 57%) and hypoproteinemia (plasma total protein concentration, 2.8 g/dL; reference range, 6.0 to 7.5 g/dL) and indicated that the dog was thrombocytopenic (110 X 103 platelets/μL; reference range, 211 X 103 platelets/μL to 621 X 103 platelets/μL).2 Results of the serum biochemical analyses indicated moderately high liver enzyme activities, hypoalbuminemia (0.9 g/ dL; reference range, 2.3 to 3.1 g/dL), hypoglobulinemia (1.4 g/dL; reference range, 2.7 to 4.4 g/dL), hypocalcemia, (6.5 mg/dL; reference range, 9.1 to 11.7 mg/dL), hypocholesterolemia (89 mg/dL; reference range, 135 to 278 mg/dL), hypomagnesemia (1.1 mg/dL; reference range, 1.6 to 2.4 mg/dL), hyponatremia (138 mEq/L; reference range, 142 to 152 mEq/L), hypokalemia (2.6 mEq/L; reference range, 3.9 to 5.1 mEq/L), and hypochloremia (105 mEq/L; reference range, 110 to 124 mEq/L).2 Plasma and whole blood taurine concentrations were within reference ranges. During the blood-type crossmatching procedure, microfilaria were detected. Thoracic radiography revealed a multifocal, patchy, interstitial pulmonary pattern. The left cranial pulmonary artery was mildly distended and did not taper as expected in a clinically normal dog. The cardiac silhouette appeared normal.

Following the initial whole blood transfusion on day 2, Hct increased to 28%. Echocardiographic abnormalities included mild myocardial failure with a fractional shortening of 31% (reference range, > 34%3) and a moderately volume-overloaded left ventricle (diastolic left ventricular internal dimension, 4.22 cm [reference limit, < 3.8 cm]; systolic left ventricular internal dimension, 2.89 cm [reference limit,3 < 2.4 cm]); heartworms were visible in the right pulmonary artery. Another ECG was performed (Figure 1).

Figure 1—
Figure 1—

Lead II ECG tracing obtained after a whole blood transfusion in a 3-year-old dog evaluated for emaciation, recumbency, and dull mentation associated with a 1-month history of malnutrition through neglect. The trace is indicative of sinus arrhythmia with first-degree atrioventricular block. Notice the regularly irregular rhythm (heart rate, approx 100 beats/min). No ventricular premature depolarizations are present. The QRS complexes are low voltage (0.25 mV); the PR and QT intervals are 0.15 seconds and 0.3 to 0.35 seconds, respectively. Paper speed = 50 mm/s; 1 mV = 10 mm.

Citation: Journal of the American Veterinary Medical Association 230, 7; 10.2460/javma.230.7.1002

ECG Interpretation

Electrocardiography was performed following whole blood transfusion on day 2 and revealed a regularly irregular rhythm with a heart rate of approximately 100 beats/min (Figure 1). As compared with the initial ECG findings on day 1, ventricular premature depolarizations were no longer present. The rhythm was interpreted as a sinus arrhythmia with first-degree atrioventricular block. On the ECG tracing, the QRS complexes were of low voltage (0.25 mV; reference range, 0.5 to 3.0 in large-breed dogs4). The PR interval was mildly prolonged (0.15 seconds; reference range, 0.06 to 0.13), and the QT interval was long (0.30 to 0.35 seconds; reference range, 0.15 to 0.25, depending on heart rate4).

The treatment protocol for the dog included IV administration of magnesium sulfate, dextrose, and hetastarch; IV fluid therapy; whole blood and fresh frozen plasma transfusions; dopamine infusion; administration of ampicillin, enrofloxacin, famotidine, sucralfate, and fenbendazole; and a high-fat, high-protein canned dog food. The dog improved considerably during the 8 days following admission to the hospital. After 8 days, the dog's anemia was less pronounced (Hct, 25%) and plasma total protein and serum albumin concentrations were increased (5.9 and 2.9 g/dL, respectively), compared with initial findings; all electrolyte values were within reference ranges. The dog was able to stand, urinate and defecate normally, and walk short distances, and its discharge from hospital was arranged. At this time, the dog was receiving daily quantities of food equivalent to 1.5 to 2 times its maintenance daily energy requirements, and the owners were instructed to continue oral administration of enrofloxacin, ampicillin, famotidine, sucralfate, and a taurine supplement at home. An ECG was performed prior to discharge on day 8 and revealed a regularly irregular rhythm with a heart rate of approximately 120 beats/min (Figure 2). The rhythm was interpreted as a sinus arrhythmia. The voltage of each QRS complex (0.9 mV) was within reference range.4 The PR interval was 0.12 seconds, and the QT interval was also normalized at 0.20 to 0.22 seconds.

Figure 2—
Figure 2—

Lead II ECG tracing obtained from the dog in Figure 1 at the time of discharge from the hospital following 8 days of treatment. The trace is indicative of sinus arrhythmia. Notice the regularly irregular rhythm (heart rate, approx 120 beats/min). Voltage of the QRS complexes was within reference range (0.9 mV4); the PR and QT intervals were 0.12 seconds and 0.2 to 0.22 seconds, respectively. Paper speed = 50 mm/s; 1 mV = 10 m m.

Citation: Journal of the American Veterinary Medical Association 230, 7; 10.2460/javma.230.7.1002

The owners moved from the area, and the recommended recheck examinations and heartworm extraction were performed at the University of Pennsylvania. Echocardiography performed 1 month following initial discharge (ie, day 40) revealed that left ventricular chamber dimensions were within reference limits and that the fractional shortening had increased (38%). Electrocardiography was also performed, and examination of the ECG trace revealed a regular sinus rhythm with a heart rate of approximately 130 beats/min (Figure 3). All ECG variables were within reference limits. Heartworm extraction and adulticide treatment were successful and without complication.

Figure 3—
Figure 3—

Lead II ECG tracing obtained from the dog in Figure 1 obtained at a recheck examination (performed at another institution) 1 month after initial discharge. Notice the regular rhythm (heart rate, approx 130 beats/min). All ECG variables are within reference limits. Paper speed = 50 mm/s; 1 mV = 10 mm.

Citation: Journal of the American Veterinary Medical Association 230, 7; 10.2460/javma.230.7.1002

Discussion

In animals, clinical signs of malnutrition result from inadequate nutritional intake and the predominance of catabolic processes and progressive wasting of fat and muscle protein body reserves. The effects of malnutrition are further complicated by electrolyte disorders and mineral or vitamin deficiencies. Regardless of its cause, malnutrition in humans and other animals affects cardiac function, cardiac muscle mass, and the electrical properties of myocardium.5–15 Atrophy and degeneration of the muscle fibers and myocytolysis with fat infiltration and fibrosis are evident histologically in heart tissue from animals with malnutrition.8,9

Several echocardiographic investigations5–8 of humans with malnutrition or anorexia nervosa have revealed that the cardiac muscle mass (measured as left ventricular mass) is decreased (proportional to the degree of malnutrition); the muscle mass can be normalized with supportive care and nutritional rehabilitation. In other studies6,7,10 of children with malnutrition, functional abnormalities with decreased shortening fraction and ejection fractions have been detected echocardiographically. Whether these distinct pathologic and electrophysiologic changes can be attributed directly to the cardiovascular abnormalities associated with severe malnutrition (eg, hypotension, cardiac arrhythmias, cardiomyopathy, cardiac failure, and sudden death) remains controversial6,9,11,12 However, there is evidence to indicate that successful recovery of nutritional status results in the return of normal cardiac function and size.5–12

Electrocardiographic changes in humans with severe malnutrition were reported as early as 1941 during World War II.13 Similar ECG changes have been detected in humans, rats, and other animals with malnutrition.13–15 Findings have included sinus bradycardia; markedly low amplitudes of the P waves, QRS complexes, and T waves; and long QT intervals.13–15 Administration of a high-protein diet caused a remarkable improvement in the clinical and ECG features of those patients.13–15 The decrease of the QRS amplitude, relative to that in clinically normal individuals, is one of the most important ECG changes identified in the aforementioned studies and may be attributable to the loss of myocardial mass.14 Hypocalcemia and hypokalemia, which are common abnormalities in animals with malnutrition, are associated with cardiac repolarization alterations and prolonged QT intervals.8 In humans, a long QT interval is associated with increased risk for arrhythmogenesis and development of ventricular arrhythmias with an increased risk of death; however, such associations are not common in other species.8

For the dog of this report, the most notable ECG abnormality was the presence of low-voltage QRS complexes, which resolved following appropriate nutritional treatment. Typically, low-voltage QRS complexes in dogs are attributable to pericardial effusion or an increased distance of the heart from the recording electrode leads (eg, as a result of obesity or a large thoracic wall). Other extracardiac causes of low-voltage QRS complexes are emphysema, pneumothorax, or pleural effusion.16 However, none of these factors were present in the dog of this report. The dog was severely emaciated and had muscle wasting and clinical signs of severe malnutrition with electrolyte and mineral depletions. On the basis of previous studies,13–15 the cause of the low-voltage QRS complexes in the dog was attributed to the complex catabolic processes of malnutrition and a secondary decrease in heart muscle mass.

In all mammalian species, the QT interval varies inversely with the heart rate—the faster the heart rate, the shorter the interval.16 The dog of this report had a long QT interval, which can develop with hypocalcemia, hypokalemia, quinidine toxicosis, ethylene glycol poisoning, strenuous exercise, hypothermia, and CNS disorders.16 Prolongation of the QT interval does not appear to be as deleterious in veterinary patients as in humans, in whom it is associated with development of ventricular arrhythmias and increased risk of death.16 Hypokalemia and hypocalcemia may have been the cause of the long QT interval in the dog of this report, and treatment included correction of electrolyte imbalances.

On the basis of the initial echocardiographic findings and blood pressure measurements, the dog of this report may have had poor systolic function and failure to move blood forward through the circulatory system because of the negative effects of malnutrition. It is likely that prolonged semistarvation negatively affects the myocardium, for which functional compensation may be achieved temporarily. However, decompensation can occur under conditions of additional stress, such as electrolyte disorders, heartworm disease, or sepsis. Interestingly, the second echocardiogram obtained 1 month following the initial discharge from the hospital indicated that the dog's systolic function had improved (as determined by shortening fraction) after nutritional rehabilitation, provision of supportive care, and administration of antimicrobials. This finding is consistent with data obtained in other studies5–12 of cardiac changes with malnutrition and subsequent recovery.

Regardless of its etiology, malnutrition is a complex phenomenon that can cause critical loss of heart and skeletal muscle and can be further complicated by electrolyte imbalances and mineral or vitamin deficiencies. Special precautions must be taken during treatment of animals with malnutrition because of the possibilities of development of arrhythmias or other abnormalities commonly associated with severe malnutrition (eg, sepsis) and sudden death. Cardiac evaluation, electrolyte disturbance correction, and appropriate nutritional therapy should be considered in the management of animals with severe malnutrition.

References

  • 1

    Ettinger SJ. The physical examination of the dog and cat. In:Ettinger SJ, Feldman EC, ed.Textbook of veterinary internal medicine. 6th ed. Philadelphia: Saunders, 2005;6.

    • Search Google Scholar
    • Export Citation
  • 2

    Latimer KS, Mahaffey EA, Prasse KW. Quality control, test validity, and reference values. In:Duncan & Prasse's veterinary laboratory medicine, clinical pathology. 4th ed. Ames, Iowa: Iowa State Press, 2003;338341.

    • Search Google Scholar
    • Export Citation
  • 3

    Kittleson MD, Kienle RD. Echocardiography. In:Small animal cardiovascular medicine. St Louis: Mosby Inc, 1998;104, 378.

  • 4

    Tilley LP. Canine electrocardiographic interpretation. In:Essentials of canine and feline electrocardiography. St Louis: CV Mosby Co, 1979;58.

    • Search Google Scholar
    • Export Citation
  • 5

    Ocal B, Unal S, Zorlu P, et al. Echocardiographic evaluation of cardiac functions and left ventricular mass in children with malnutrition. J Paediatr Child Health 2001;37:1417.

    • Search Google Scholar
    • Export Citation
  • 6

    Phornphatkul C, Pongprot Y, Suskind R. Cardiac function in malnourished children. Clin Pediatr (Phila) 1994;33:147154.

  • 7

    Kothari SS, Patel TM, Shetalwad AN, et al. Left ventricular mass and function in children with severe protein energy malnutrition. Int J Cardiol 1992;35:1925.

    • Search Google Scholar
    • Export Citation
  • 8

    Olivares JL, Vazquez M, Rodriguez G, et al. Electrocardiographic and echocardiographic findings in malnourished children. J Am Coll Nutr 2005;24:3843.

    • Search Google Scholar
    • Export Citation
  • 9

    Gelb BD, Abdenur J. Metabolic heart disease. In:Garson A, Bricker TJ, Fisher DJ, et al, eds. The science and practice of pediatric cardiology. 2nd ed. Baltimore: The Williams & Wilkins Co, 1998;1913.

    • Search Google Scholar
    • Export Citation
  • 10

    Singh GR, Malathi KE, Kasliwal RR, et al. An evaluation of cardiac function in malnourished children by non-invasive methods. Indian Pediatr 1989;26:875881.

    • Search Google Scholar
    • Export Citation
  • 11

    McLaren DS. Protein energy malnutrition (PEM): classification, pathogenesis, prevalence, prevention. In:McLaren DS, Burman D, ed.Textbook of pediatric nutrition. 3rd ed. Edinburgh: Churchill Livingstone Inc, 1982;103113.

    • Search Google Scholar
    • Export Citation
  • 12

    Figueroa-Colon R. Clinical and laboratory assessment of the malnourished child. In:Suskind RM, Suskind LL, ed.Textbook of pediatric nutrition. New York: Raven Press, 1993;191203.

    • Search Google Scholar
    • Export Citation
  • 13

    Simonson E, Henschel A, Keys A. The electrocardiogram of man in semistarvation and subsequent rehabilitation. Am Heart J 1948;35:584602.

    • Search Google Scholar
    • Export Citation
  • 14

    Pissaia O, Marcos R, Oliveira J. The heart in protein-calorie malnutrition in rats: morphological, electrophysiological and biochemical changes. J Nutr 1980;110:20352044.

    • Search Google Scholar
    • Export Citation
  • 15

    Gopalan C, Srikantiah SG, Venkatachalam PS. Electrocardiographic changes in severe malnutrition. Indian J Med Res 1955;43:1521.

  • 16

    Fox PR, Sisson D, Moise SN. Diagnostic methods. In:Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: WB Saunders Co, 1999;90, 9798.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Lead II ECG tracing obtained after a whole blood transfusion in a 3-year-old dog evaluated for emaciation, recumbency, and dull mentation associated with a 1-month history of malnutrition through neglect. The trace is indicative of sinus arrhythmia with first-degree atrioventricular block. Notice the regularly irregular rhythm (heart rate, approx 100 beats/min). No ventricular premature depolarizations are present. The QRS complexes are low voltage (0.25 mV); the PR and QT intervals are 0.15 seconds and 0.3 to 0.35 seconds, respectively. Paper speed = 50 mm/s; 1 mV = 10 mm.

  • Figure 2—

    Lead II ECG tracing obtained from the dog in Figure 1 at the time of discharge from the hospital following 8 days of treatment. The trace is indicative of sinus arrhythmia. Notice the regularly irregular rhythm (heart rate, approx 120 beats/min). Voltage of the QRS complexes was within reference range (0.9 mV4); the PR and QT intervals were 0.12 seconds and 0.2 to 0.22 seconds, respectively. Paper speed = 50 mm/s; 1 mV = 10 m m.

  • Figure 3—

    Lead II ECG tracing obtained from the dog in Figure 1 obtained at a recheck examination (performed at another institution) 1 month after initial discharge. Notice the regular rhythm (heart rate, approx 130 beats/min). All ECG variables are within reference limits. Paper speed = 50 mm/s; 1 mV = 10 mm.

  • 1

    Ettinger SJ. The physical examination of the dog and cat. In:Ettinger SJ, Feldman EC, ed.Textbook of veterinary internal medicine. 6th ed. Philadelphia: Saunders, 2005;6.

    • Search Google Scholar
    • Export Citation
  • 2

    Latimer KS, Mahaffey EA, Prasse KW. Quality control, test validity, and reference values. In:Duncan & Prasse's veterinary laboratory medicine, clinical pathology. 4th ed. Ames, Iowa: Iowa State Press, 2003;338341.

    • Search Google Scholar
    • Export Citation
  • 3

    Kittleson MD, Kienle RD. Echocardiography. In:Small animal cardiovascular medicine. St Louis: Mosby Inc, 1998;104, 378.

  • 4

    Tilley LP. Canine electrocardiographic interpretation. In:Essentials of canine and feline electrocardiography. St Louis: CV Mosby Co, 1979;58.

    • Search Google Scholar
    • Export Citation
  • 5

    Ocal B, Unal S, Zorlu P, et al. Echocardiographic evaluation of cardiac functions and left ventricular mass in children with malnutrition. J Paediatr Child Health 2001;37:1417.

    • Search Google Scholar
    • Export Citation
  • 6

    Phornphatkul C, Pongprot Y, Suskind R. Cardiac function in malnourished children. Clin Pediatr (Phila) 1994;33:147154.

  • 7

    Kothari SS, Patel TM, Shetalwad AN, et al. Left ventricular mass and function in children with severe protein energy malnutrition. Int J Cardiol 1992;35:1925.

    • Search Google Scholar
    • Export Citation
  • 8

    Olivares JL, Vazquez M, Rodriguez G, et al. Electrocardiographic and echocardiographic findings in malnourished children. J Am Coll Nutr 2005;24:3843.

    • Search Google Scholar
    • Export Citation
  • 9

    Gelb BD, Abdenur J. Metabolic heart disease. In:Garson A, Bricker TJ, Fisher DJ, et al, eds. The science and practice of pediatric cardiology. 2nd ed. Baltimore: The Williams & Wilkins Co, 1998;1913.

    • Search Google Scholar
    • Export Citation
  • 10

    Singh GR, Malathi KE, Kasliwal RR, et al. An evaluation of cardiac function in malnourished children by non-invasive methods. Indian Pediatr 1989;26:875881.

    • Search Google Scholar
    • Export Citation
  • 11

    McLaren DS. Protein energy malnutrition (PEM): classification, pathogenesis, prevalence, prevention. In:McLaren DS, Burman D, ed.Textbook of pediatric nutrition. 3rd ed. Edinburgh: Churchill Livingstone Inc, 1982;103113.

    • Search Google Scholar
    • Export Citation
  • 12

    Figueroa-Colon R. Clinical and laboratory assessment of the malnourished child. In:Suskind RM, Suskind LL, ed.Textbook of pediatric nutrition. New York: Raven Press, 1993;191203.

    • Search Google Scholar
    • Export Citation
  • 13

    Simonson E, Henschel A, Keys A. The electrocardiogram of man in semistarvation and subsequent rehabilitation. Am Heart J 1948;35:584602.

    • Search Google Scholar
    • Export Citation
  • 14

    Pissaia O, Marcos R, Oliveira J. The heart in protein-calorie malnutrition in rats: morphological, electrophysiological and biochemical changes. J Nutr 1980;110:20352044.

    • Search Google Scholar
    • Export Citation
  • 15

    Gopalan C, Srikantiah SG, Venkatachalam PS. Electrocardiographic changes in severe malnutrition. Indian J Med Res 1955;43:1521.

  • 16

    Fox PR, Sisson D, Moise SN. Diagnostic methods. In:Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: WB Saunders Co, 1999;90, 9798.

    • Search Google Scholar
    • Export Citation

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