Hiroshi Kuida

Brisket disease: II. Clinical features and hemodynamic observations in altitude-dependent right heart failure of cattle

Abstract In cattle grazing during the summer months at altitudes between 8,000 and 12,000 feet (2,500 to 3,700 meters) in Utah and Colorado severe congestive heart failure develops. The disease is apparently the consequence of severe pulmonary hypertension which develops in this species in response to moderate altitudes. This form of chronic mountain sickness has many similarities to pulmonary hypertensive heart disease in man. It differs from Monges disease in certain significant aspects. It is assumed that the peculiar structure of the pulmonary vascular bed in this species causes an excessive vasoconstrictive response at a reduction in partial pressure of oxygen which is still easily tolerated by man.

Heart failure in atrial septal defect

Abstract The hemodynamic data procured in thirtytwo adults with large atrial septal defects are reviewed and compared with those from six cases in children in whom atrial septal defect was complicated by pulmonary stenosis. Elevated right atrial pressure was a common finding in the adults. In the absence of mitral stenosis or constrictive pericarditis, elevation of right atrial pressure in large atrial septal defects may be considered a sign of left ventricular failure. Right ventricular failure in atrial septal defect is characterized by a decrease in the left-to-right shunt, appearance of a right-to-left shunt and a decrease in right ventricular forward output. All this occurs at normal pressures in the common atrium. Biventricular failure, occurring together or in sequence, is a common complication of atrial septal defect in the adult.

Hemodynamic effects of exercise in patients with aortic stenosis

Abstract Hemodynamic data obtained by right and left heart catheterization at rest and during exercise in thirty-two patients with aortic stenosis were reviewed. Eighteen patients had either minimal or no aortic regurgitation (group I) and fourteen patients had moderate to moderately severe aortic regurgitation (group II). The mean systolic pressure gradient (ΔP) across the aortic valve decreased or remained unchanged during exercise in eleven of eighteen patients in group I and in nine of fourteen patients in group II. Net forward aortic valve systolic flow (AVSF) increased during exercise in fourteen of eighteen patients in group I and in thirteen of fourteen patients in group II. Thus, in some patients the change in ΔP during exercise appears to be at variance with the predictability implied by the Gorlin equation which states that ΔP should be directly related to (AVSF) 2 . It is unlikely that this discrepancy can be explained on the basis of a systematic measuring error involving one or more of the various factors in the equation. This suggests that the aortic valve may not behave as a fixed orifice under all hemodynamic conditions, and that orifice hydraulics might be different depending on the mechanics of contraction. Average cardiac index (CI) was 2.5 L. per minute per M 2 . at rest and 3.8 L. per minute per M 2 . during exercise for patients in group 1, and 2.2 L. per minute per M 2 . at rest and 3.9 L. per minute per M 2 . during exercise for patients in group 2. Arterial and left ventricular systolic and diastolic pressures increased, and systemic resistance decreased during exercise. Thus, resting cardiac output is maintained and it increases during exercise at the expense of marked elevation in both systolic and diastolic pressures in the left ventricle. An analysis of the relationship between stroke work index (SWI) and left ventricular end diastolic pressure (LV edp ) in patients from group I revealed, in general, two types of responses to exercise. Six patients had an increase in SWI averaging 39 per cent associated with a 67 per cent increase in LV edp . In sharp contrast, ten other patients demonstrated an increase in SWI averaging only 1.3 per cent whereas LV edp increased by an average of 129 per cent. It is apparent therefore that the response to exercise makes it possible to separate patients with remaining myocardial reserve from those without. Thus, exercise data in patients with aortic stenosis provide objective, quantitative information useful in making a decision when and if to perform corrective surgery.

The cardiac output in paget's disease before and after treatment with cortisone

Abstract 1.1. Observations on the cardiac output have been made in six patients with extensive Pagets disease before and during treatment with large doses of cortisone. 2.2. In all cases, cardiac output was elevated before treatment. High doses of cortisone for a sufficient duration, more than three days and less than nine days, produced a pronounced fall to normal levels. Serum alkaline phosphatase levels changed in the same direction as the cardiac output. 3.3. Cortisone had no consistent effect on oxygen consumption, large vessel hematocrit, total blood volume, pulse pressure or mean arterial pressure. Cortisone therapy resulted in a pronounced drop in pulse rate in three of the six patients studied. 4.4. The mechanism through which cortisone exerts its effect on cardiac output in Pagets disease was not elucidated by these studies.

Effects of prostaglandins F2a and E2 on the bovine circulation.

Summary The effects of PGF2α and PGE2 on the pulmonary and systemic circulations were studied in unanesthetized calves. PGF2α, average dose 2.1 μg/kg, injected into the pulmonary artery resulted in a significant increase in PA pressure and fall in CO whereas FA pressure, LV end diastolic pressure, HR, blood gases and pH were not significantly altered. PGE2, average dose 1.9 μg/kg, injected into the pulmonary artery resulted in a significant decrease in FA pressure, increase in HR and a small but significant increase in PA pressure whereas LV end diastolic pressure, CO, blood gases and pH were not significantly altered. Thus, this study indicates that in the bovine PGF2α causes pulmonary vasoconstriction and PGE2 causes systemic vasodilatation. The authors are indebted to Dr. J. E. Pike of the Upjohn Company for generous supplies of prostaglandins. The technical assistance of Mr. Don Anton and Filimon Ukradyha, PhD, is greatly appreciated.

BRISKET DISEASE. III. SPONTANEOUS REMISSION OF PULMONARY HYPERTENSION AND RECOVERY FROM HEART FAILURE.

Previous reports from this laboratory have dealt with the ecologic, pathologic, clinical, and pathophysiologic features of brisket disease (1, 2). On the basis of these studies brisket disease may be defined as altitude-dependent, pulmonary, hypertensive heart disease in cattle of the species Bos taiurus. Briefly, the disease in Utah occurs primarily in young calves usually during their first exposure to conditions existing on summer ranges at elevations between 8,000 and 11,000 feet. Typical findings in animals suffering from brisket disease are outlined in Table 1. It was observed that a significant number of animals with acute brisket disease recovered when removed from the mountainous ranges and brought to Salt Lake City, Utah (elevation 4,500 feet). This observation prompted an investigation of the nature, magnitude, and time course of changes in various physiologic parameters associated with clinical recovery. The demonstration of dramatic remission from pulmonary hypertension and improvement in over-all cardiovascular function provides the basis for this report.

Effect of Alterations in Vasomotor Tone on Pressure-Flow Relationships in the Totally Perfused Dog

The technic of total body perfusion with a pump oxygenator system has been used to extend pressure flow studies to the circulation as a whole. The effect of alterations in vasomotor tone on both total peripheral resistance and pressure flow relationships has been investigated by surgical ablation of the central nervous system or administration of vasoactive drugs. Certain aspects of the results obtained are discussed in relation to the concept of critical closing pressures.

Clinical and physiologic sequelae of large ventricular septal defects.

Abstract The clinical and hemodynamic data in twenty-nine patients with large ventricular septal defects are analyzed. Evidence of heart failure is uncommon in those with pulmonary vascular disease and/or pulmonic stenosis alone, in contrast to those in whom certain other additional congenital lesions are present. These data are analyzed in terms of a physiologically single ventricle which exists when a large ventricular septal defect is present. Obligatory beat to beat synchronicity of the right ventricular and systemic arterial systolic pressure is discussed and its use in the diagnosis of the physiologically single ventricle in man outlined. Evidence is presented that in the face of a physiologically single ventricle, ventricular failure is most likely to occur when a volume or flow load is present in addition to right ventricular hypertension. The evolution and hemodynamic recognition of ventricular failure in the face of a physiologically single ventricle is discussed.

Patent ductus arteriosus complicated by heart failure: Classification based on clinical and serial hemodynamic studies

A heterogeneous group of four patients with patent ductus arteriosus and heart failure is described and the data from their serial hemodynamic studies are discussed. The evolution and etiology of heart failure in patients with patent ductus arteriosus is variable and is discussed in terms of a classification based on both the size of the defect and the degree of coexisting pulmonary vascular resistance. The hemodynamic evolution of heart failure is shown to be a relatively slow process. Coexisting features which may modify the evolution of failure are semilunar valvular insufficiency, a coexisting ventricular septal defect and possibly the volume of packed red cells.

Effect of Endotoxin on Vascular Reactivity to Epinephrine in the Perfused Dog Forelimb and Lung.

Summary Experiments were carried out on isolated perfused lungs and forelimbs of adult dogs. There was no significant change in vascular response to epinephrine following injection of endotoxin.