Localized pericardial effusion and right-sided heart tamponade: complications of cardiac surgery in a Hanford miniature pig.
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Biomedical subjects
Publications and source records attributed to M D Kittleson.
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Between October 1986 and September 1988, 37 cats with moderate to severe idiopathic myocardial failure (dilated cardiomyopathy) were evaluated prospectively. Low plasma taurine concentration and diet history including foods that can cause taurine deficiency were documented in most of the cats. Comparison with a retrospectively studied population of 33 cats with dilated cardiomyopathy diagnosed between 1980 and 1986 demonstrated that the clinical and historical findings in the 33 retrospectively studied cats were similar to those in the 37 cats studied prospectively. Clinical findings in the 2 groups were also similar to findings previously reported in the literature. Because clinical findings and diet history were similar in the prospective and retrospective groups, we believe that many cats in the latter group had diet-induced taurine deficiency. These findings support the conclusion that most cases of dilated cardiomyopathy in cats have a common etiopathogenesis related to diet and as such are preventable.
Between October 1986 and September 1988, 37 cats with moderate to severe idiopathic myocardial failure (dilated cardiomyopathy) were evaluated. Clinical management of these cats was similar to that described in the literature, except that it also included administration of 500 or 1,000 mg of the sulfur amino acid, taurine per day. Early death (death within the first 30 days of treatment) occurred in 14 (38%) cats. One cat was lost to follow-up evaluation. Twenty-two cats (59%) had marked clinical and echocardiographic improvement and survived longer than 240 days. In all but 1 cat, the observed improvement in echocardiographic measurements persisted. Hypothermia and thromboembolism were positively associated with an increased risk of early death. Administration of digoxin did not significantly affect survival. All 22 cats that survived greater than 30 days remained clinically stable despite withdrawal of all medications except taurine. Administration of taurine was eventually discontinued in 20 of the 22 cats and adequate taurine intake was thereafter provided for in the food. The clinical response and 1-year survival rate of 58% (21 of 36 cats with a known outcome) in the taurine-treated group represents a marked improvement, compared with a 1-year survival rate of 13% (4 of 31 cats with a known outcome) in a retrospectively evaluated population of 33 cats with dilated cardiomyopathy.
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Milrinone has been studied in a variety of situations. In experimental dogs it has been documented to increase contractility to a similar degree as beta-receptor agonists and to produce mild arteriolar dilation in dogs. In canine patients with heart failure, milrinone produces demonstrable improvement in echocardiographic ventricular function and hemodynamic variables. In addition, it improves clinical signs in these patients, improving their quality of life. Milrinone is superior to digoxin as evidenced by the improvement in clinical signs noted in dogs that were unresponsive or no longer responding to digoxin administration. There is no doubt that milrinone improves short-term prognosis and in so doing prolongs life. Many of the patients that the author has observed would not have gone home without the benefits of milrinone. Milrinone's effects on long-term survival cannot be assessed, but its effects on survival time are certainly not dramatic enough to be evident without a comparison population. Therefore, milrinone administration should be considered palliative, as is administration of all other cardiovascular medications for heart failure. In addition to its beneficial effects, milrinone also appears to be relatively safe when compared with the alternative of digoxin administration. Fatal events attributable to milrinone administration are rare, and those directly attributable to enhanced ventricular arrhythmia can generally be avoided by monitoring an electrocardiogram after initial milrinone administration commences. Milrinone does not increase the incidence of sudden death in Doberman Pinschers. It is possible that a small number of dogs with mitral regurgitation may develop mitral chordal rupture. For this reason and possibly others, milrinone probably will not be indicated in early heart failure due to mitral regurgitation when heart failure is readily responsive to diuretic administration. The risk-to-benefit ratio turns markedly in the favor of milrinone administration in the dog with mitral regurgitation that is partially or completely refractory to other cardiovascular drugs. Milrinone appears to be a more effective and safer positive inotrope for long-term treatment of dogs with congestive heart failure than drugs currently available. The author and all the investigators involved in the milrinone clinical trials hope that it will soon be available for use by the veterinary community.
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Anesthesia induced by use of a combination of xylazine, ketamine, and halothane, under conditions of spontaneous and mechanically controlled ventilation, was evaluated in 5 llamas positioned in dorsal recumbency. Using chronically implanted catheters, systemic arterial blood pressure, pulmonary arterial pressure, right atrial pressure, heart rate and rhythm, cardiac output, blood pH and gas tensions, body temperature, and respiratory rate were measured before anesthesia induction (baseline), throughout the anesthetic period, and for 1 hour into the recovery period. During anesthesia, llamas undergoing spontaneous ventilation developed hypercapnia and respiratory acidosis. Cardiovascular function was decreased during both types of ventilation. The combination of xylazine, ketamine, and halothane in various doses and 2 ventilation procedures (spontaneous and controlled) provided a reliable method for general anesthesia in llamas, but marked cardiovascular depression developed during anesthesia maintenance with halothane. Spontaneous ventilation resulted in potentially clinically important respiratory acidosis.
Thousands of pet cats die each year with dilated cardiomyopathy, the cause of which is unknown. Although taurine is present in millimolar concentrations in the myocardium of all mammals, taurine depletion has not previously been associated with a decrease in myocardial function in any species. In this study, low plasma taurine concentrations associated with echocardiographic evidence of myocardial failure were observed in 21 cats fed commercial cat foods and in 2 of 11 cats fed a purified diet containing marginally low concentrations of taurine for 4 years. Oral supplementation of taurine resulted in increased plasma taurine concentrations and was associated with normalization of left ventricular function in both groups of cats. Since myocardial concentrations of taurine are directly related to plasma concentrations and low plasma concentrations were found to be associated with myocardial failure in cats, a direct link between decreased taurine concentration in the myocardium and decreased myocardial mechanical function is proposed.
Experimental myocardial infarction of the posterolateral wall of the left ventricle was produced in dogs by injecting 80 micron microspheres into the left circumflex coronary artery to determine changes in regional myocardial function after infarction, to examine how the changes in regional myocardial function relate to the changes in global left ventricular function, and to examine the relationship between regional wall motion and wall thickening after myocardial infarction. Serial measurements of global ventricular and regional myocardial function were made in six dogs before and during 20 days after infarction, with the use of M-mode echocardiography and chronic Swan-Ganz catheter implantation. One hour after infarction, stroke volume index had decreased 49% from baseline, percent fractional shortening had decreased 52%, lateral wall motion had decreased 80%, and lateral wall thickening had decreased 100%. By 6 days after infarction, stroke volume index had increased 41% from its low point, percent fractional shortening had increased 34%, and lateral wall motion had increased 100% toward but not to baseline. Lateral wall thickening did not return following infarction. Peak and end-systolic circumferential wall stresses and systemic arterial blood pressure remained stable. End-systolic diameter increased acutely (36%) after infarction and did not change during the 20-day time period, while end-diastolic diameter gradually increased, resulting in the increase in percent fractional shortening. In conclusion, after posterolateral wall infarction, wall motion can return without an improvement in regional myocardial function, presumably because the infarcted region stiffens, allowing it to be pulled inward.(ABSTRACT TRUNCATED AT 250 WORDS)
Neurohumoral, cardiovascular, and respiratory parameters were evaluated during sustained submaximal exercise (3.2 km/h, 15 degrees elevation) in normal adult mongrel dogs. At the level of activity achieved (fivefold elevation of total body O2 consumption and threefold elevation of cardiac output), significant (P less than 0.05) increases in plasma norepinephrine and epinephrine concentration (from 150 +/- 23 to 341 +/- 35 and from 127 +/- 27 to 222 +/- 31 pg/ml, respectively) were present, as well as smaller but significant increases in plasma renin activity and plasma aldosterone concentration (from 2.2 +/- 0.3 to 3.1 +/- 0.6 ng X ml-1 X h-1 and from 98 +/- 8 to 130 +/- 6 pg/ml, respectively). Plasma arginine vasopressin increased variably and insignificantly. The cardiovascular response (heart rate, systemic arterial and pulmonary arterial pressures, left ventricular filling pressure, and calculated total peripheral and pulmonary arteriolar resistance) closely paralleled that of human subjects. Increased hemoglobin concentration was induced by exercise in the dogs. The ventilatory response of the animals was characterized by respiratory alkalosis. These data suggest similarities between canine and human subjects in norepinephrine, plasma renin activity, and plasma aldosterone responses to submaximal exercise. Apparent species differences during submaximal exertion include greater alterations of plasma epinephrine concentration and a respiratory alkalosis in dogs.
The hemodynamic response to hydralazine administration was evaluated in 6 conscious small dogs with chronic mitral regurgitation. All dogs underwent invasive and noninvasive hemodynamic monitoring before and after hydralazine administration. Cardiac output and pulmonary capillary wedge pressure were measured with a Swan-Ganz thermodilution catheter. Systemic arterial blood pressure (AP) was measured directly by inserting a needle into the femoral artery. Standard M-mode echocardiograms and thoracic radiographs were obtained. Other hemodynamic variables were calculated. Base-line hemodynamic variables were altered severely in all dogs. Hydralazine decreased mean arterial blood pressure from 104 +/- 18 (mean +/- SD) to 78 +/- 12 mm of Hg (P less than 0.005), total systemic resistance index from 2,946 +/- 625 to 1,261 +/- 420 dynes-s-cm-5m2 (P less than 0.005), and pulmonary capillary wedge pressure from 40 +/- 5 to 26 +/- 3 mm of Hg, (P less than 0.005). Cardiac index increased from 2.92 +/- 0.72 to 5.36 +/- 1.67 L/min/m2 of body surface area (P less than 0.005). Mixed venous oxygen tension (PvO2) increased from 28.4 +/- 4.3 to 41.2 +/- 5.2 mm of Hg (P less than 0.001). Pulmonary edema resolved, as determined on thoracic radiographs. Mixed venous oxygen tension correlated well with the cardiac index (r = 0.92; P less than 0.001). It was concluded that hydralazine administration caused a small decrease in end diastolic diameter (4.8 +/- 0.9 to 4.5 +/- 0.8 cm, P less than 0.05) and end systolic diameter (2.6 +/- 0.8 to 2.3 +/- 0.7 cm, P less than 0.05). Fractional shortening and heart rate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
Digoxin administration (0.22 mg/m2 of body surface BID) to 10 large-breed dogs with congestive cardiomyopathy increased shortening fraction more than 5.5% in 4 of the dogs. This group of dogs lived longer than the group that did not have a positive inotropic response to digoxin. Heart rate decreased in both groups of dogs. Base-line jugular PVO2 were low in all dogs. Jugular PVO2 decreased significantly in the group that did not respond to digoxin, presumably because of decreased cardiac output. Jugular PVO2 consistently increased in dogs that had a positive inotropic response to digoxin. Base-line shortening fraction, heart rate, and PVO2 did not predict which dogs would respond to digoxin. Serum digoxin concentrations were consistently between 1.5 and 2.5 ng/ml. It was concluded that digoxin administration is not efficacious in all dogs with congestive cardiomyopathy and that the positive inotropic response is not predicted by base-line shortening fraction, heart rate, or jugular PVO2. Dogs that do respond to digoxin usually live longer than those that do not. Jugular PVO2 can be used to separate dogs that do respond from dogs that do not respond to digoxin as long as the base-line PVO2 is low. The negative chronotropic effects of digoxin may be detrimental to dogs that do not have a positive inotropic effect from digoxin.
Milrinone is a recently synthesized bypyridine compound with positive inotropic and arteriolar dilating properties in persons and experimental animals. To examine the efficacy and safety of milrinone to treat myocardial failure in dogs, dogs with myocardial failure were selected from the patient populations of 3 veterinary hospitals. Progressively increased dosages of milrinone, from 0.05 to 1.0 mg/kg of body weight, were administered over 14 days, and cardiac responses, as determined by M-mode echocardiography, and clinical responses were recorded. An effective dosage of milrinone was identified for each dog and administered for 4 weeks to evaluate the stability of the cardiac response. A randomized blinded study of drug vs nondrug capsule or nondrug elixer (designated placebo) was performed at the end of 4 weeks to eliminate possible effects of investigator bias or spontaneous regression of the disease. The duration of drug effect was determined by evaluating echocardiographic measurements of left ventricular function for 12 hours after drug administration. Echocardiographic evaluation of left ventricular function improved in dogs given milrinone. The effective dosage was between 0.5 and 1.0 mg/kg. Tolerance to milrinone did not develop during the 4-week study. In dogs given placebo during the randomized blinded study, echocardiographic values decreased significantly. Dogs that were given milrinone remained echocardiographically stable. During the study, 6 dogs improved clinically, 5 remained the same, 1 had a decrease in exercise tolerance, 1 died of severe heart failure, and 1 died of hypoadrenocorticism. Ventricular tachydysrhythmia was exacerbated in 2 dogs, but was not treated.(ABSTRACT TRUNCATED AT 250 WORDS)