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Biomedical subjects

J M Reimer

Publications and source records attributed to J M Reimer.

23 records · Page 2Linked to original sources

Effect of high-dose dopamine on urine output in newborn infants.

To achieve adequate arterial BP, adequate capillary filling time, and adequate peripheral pulses, hypotensive newborn infants often require higher doses of dopamine that reportedly reduce urine output in adults. Whether these larger doses of dopamine also reduce urine output in newborns is not known. Therefore, we determined the effects of administering high-dose dopamine (more than 20 micrograms/kg X min) on the urine output of 15 newborn infants. Five infants were studied prospectively and ten retrospectively. In the prospective study, urine output was determined as the dose of dopamine was increased; in the retrospective study, urine output was determined as the infants were being weaned from high doses of dopamine. Both data sets demonstrate that administering high-dosage dopamine does not reduce the urine output of sick newborn infants. Therefore, we conclude that doses of dopamine previously reported to decrease urine output in adults do not do so in sick newborn infants. Consequently, when necessary, high doses of dopamine may be used in sick newborn infants to achieve cardiovascular stability without reducing urine output.

Birth Weight↗

Aorto-cardiac fistulas in seven horses.

This report describes the history, clinical, electrocardiographic and echocardiographic findings, treatment, outcome and post-mortem findings in seven horses with aorto-cardiac fistula. Affected horses included 5 stallions, one gelding and one mare; 2 each of the Thoroughbred, Arabian and Standardbred breeds and one Thoroughbred-cross with a mean +/- s.d. age of 12 +/- 4 years, range 6-18 years. The presenting signs were acute distress (four horses), exercise intolerance (two horses) and the lesion was detected during a routine examination in one horse. Five horses had monomorphic ventricular tachycardia on admission and one other had a history of this arrhythmia. Five horses had a characteristic continuous murmur loudest in the right fourth intercostal space. Echocardiography (six horses) and/or post-mortem examination (four horses) revealed the horses had aorto-cardiac fistulas arising from the right aortic sinus in all five horses in which the site was recorded. Two horses had ruptured aneurysmal dilatations of the aortic wall at this site. Fistulas extended into the right ventricle in four horses; the right atrium in two horses, the left ventricle in one horse, and five horses had dissecting tracts in the septal myocardium. Horses survived for periods ranging from 24 h to 4 years. Aorto-cardiac fistula should be considered in the differential diagnosis for horses presenting with acute distress, bounding arterial pulse, a right-sided continuous murmur and/or monomorphic ventricular tachycardia, particularly in middle-aged or older stallions. Echocardiography is the technique of choice for confirming the diagnosis and demonstrating accompanying cardiac changes.

Age Factors↗

An echocardiographic study of atrial fibrillation in horses: before and after conversion to sinus rhythm.

Two-dimensional and M-mode echocardiograms were recorded from 41 horses before they were successfully treated for atrial fibrillation. In addition, these examinations were performed in a subgroup of 20 horses after treatment, and the results were compared with pretreatment values. Atrial fibrillation in this group of horses was associated with a reduction of mean left ventricular fractional shortening (mean 31% +/- 5.24%), and 22 of the 41 horses were below the reference range. The remaining mean M-mode variables were within the normal reference range, although 12 horses had increased left ventricular lumen dimensions in systole, and 8 horses had decreased left ventricular ejection times. Abnormal motion of the mitral valve was present in all horses and was characterized by the absence of A peaks, which were replaced by small diastolic undulations in 55% of the horses. In horses 1 to 20, after conversion to sinus rhythm, the mean fractional shortening increased (35.34% +/- 5.4%, P = .004), but there were no significant differences in heart rate or left ventricular lumen diameters in systole or diastole. These results suggest that ventricular function may be compromised by the presence of atrial fibrillation. However, this improved after correction of the arrhythmia.

Animals↗

Treatment of atrial fibrillation in horses: new perspectives.

Forty-one horses were treated for atrial fibrillation (AF) with 22 mg/kg quinidine sulfate via nasogastric tube every 2 hours until conversion to sinus rhythm, a cumulative dose of 88 to 132 mg/kg had been administered in 2-hour increments, or the horse had adverse or toxic effects from the drug. Treatment intervals were prolonged to every 6 hours if conversion had not occurred. Digoxin was administered before treatment if the horse had a fractional shortening < or = 27% (3 horses), was prone to tachycardia (resting heart rate > or = 60 beats/min) (1 horse), or had a previous history of sustained tachycardia of over 100 beats/min during prior conversion (3 horses). Digoxin was administered during day 1 of quinidine sulfate treatment if the horse developed a sustained tachycardia of over 100 beats/min during treatment (11 horses) or on day 2 if conversion had not occurred (7 horses). Plasma quinidine concentrations within 1 hour of conversion of AF to sinus rhythm ranged from 1.7 to 7.5 micrograms/mL (mean, 4.05 +/- 1.6) and ranged from 1.7 to 4.7 micrograms/mL in 97% of horses. Most horses (92%) with plasma quinidine concentrations > 5 micrograms/mL exhibited an adverse or toxic effect of quinidine sulfate (clinical or electrocardiographic). There was no statistical association between plasma quinidine concentrations and sustained tachycardia (> 100 beats/min), diarrhea, or colic. Ataxia and upper respiratory tract stridor were significantly associated with plasma quinidine concentrations. In most instances (98%) conversion did not occur while toxic or adverse effects of quinidine sulfate were present or when plasma quinidine concentrations were > 5 micrograms/mL.

Animals↗

Idiopathic hypocalcemia in foals.

Five thoroughbred foals (4 fillies and 1 colt), all in good to excellent body condition, ranging in age from 4 days to 5 weeks at the time of onset of signs, were presented to 2 Kentucky equine hospitals from 1992 through 1996. All 5 foals presented with tachycardia, hyperhidrosis, diarrhea or a recent history of diarrhea, and muscle rigidity or stiff gait. Four of the 5 foals presented for recumbency, seizure-like activity with opisthotonos, or pronounced extensor muscle rigidity. All 5 foals were hypocalcemic. All foals either died or had euthanasia performed. None responded to oral calcium supplementation. The cause of the hypocalcemia was unknown. Different idiopathic hypocalcemia syndromes may exist in foals.

Animals↗