Harper K. Hellems

Hemodynamic Studies in Sickle Cell Anemia

Hemodynamic studies in 13 unselected patients with sickle cell anemia are reported. Twelve of these patients were also studied during mild exercise. The cardiac output at rest was elevated in all and rose significantly with exercise in 9 of the 12 patients. The importance of the increased percentage extraction of oxygen by the tissues in modifying the response of the cardiac output is discussed. The similarity of the response to exercise in the majority of these chronically anemic patients compared with the normal response is described. Included in this series is one case with secondary cor pulmonale and one case of concurrent rheumatic heart disease.

Circulatory changes in acute glomerulonephritis.

Conflicting opinions have been expressed as to the mechanism of pulmonary and peripheral congestion frequently observed in the oliguric stage of acute glomerulonephritis. Hemodynamic studies in 7 patients studied during the oliguric edematous phase of the disease demonstrated that these patients have high ventricular filling pressures associated with an increase in cardiac output and are, therefore, examples of a high output congestive state.

Coronary Blood Flow, Myocardial Oxygen Consumption, and Myocardial Metabolism in Normal and Hyperthyroid Human Subjects

The effects of thyroid hormone excess on myocardial hemodynamics and carbohydrate metabolism were determined in a group of subjects, and the findings compared with those obtained in a group of normal individuals. The results indicate that in thyrotoxicosis there tends to be an increase in coronary blood flow and myocardial oxygen consumption and a normal per cent extraction of oxygen by the myocardium. The metabolism of glucose, lactic acid, and pyruvic acid was virtually identical in the 2 groups. No relationship was demonstrable between the arterial levels of the carbohydrate substances and their extraction by the heart.

Myocardial Blood Flow and Oxygen Consumption during Postprandial Lipemia and Heparin-Induced Lipolysis

The role of the physical state of plasma as a determinant of oxygen availability to the myocardium has been investigated during the course of alimentary lipemia. After the development of substantial plasma lactescence, the coronary blood flow (nitrous oxide method) and myocardial oxygen consumption were assessed in 7 normal human subjects and repeated after heparin-induced lipolysis. The lipemic state was further contrasted with a control fasting group, comparable in age and sex. The mean coronary blood flow for 15 fasting controls was 83 ml. per 100 Gm. of left ventricle per minute with a myocardial oxygen extraction of 11.04 volumes per cent, and a myocardial oxygen consumption of 9.0 ml. per 100 Gm. of left ventricle per minute. By contrast, the mean coronary blood flow during maximal lipemia in the 7 subjects fed cream was 20 per cent below normal, with a value of 67 ml. per 100 Gm. per minute (p=< 0.01). As the extraction of oxygen was not significantly affected, the calculated myocardial oxygen consumption was proportionately reduced to 7.02 ml. per 100 Gm. per minute (p=< 0.01). A failure of the anticipated oxygen extraction increment in the face of coronary blood flow reduction suggests an impediment of blood-tissue oxygen transport during lipemia. After the administration of 60 mg. of heparin to the 7 lipemic subjects, a 65 per cent decline in plasma lactescence was observed by 45 minutes, when the coronary blood flow and myocardial oxygen consumption were elevated to 87 ml. per 100 Gm. per minute (p=< 0.05) respectively. Thus, the reduced coronary flow and myocardial oxygen consumption were restored in each instance to normal levels during the process of plasma clearing. There were no associated systemic hemodynamic changes to account for such increments. These heparin effects appear dependent on the lipemia-clearing property, for no alteration in coronary dynamics was found in 6 additional patients in whom this activity was not manifest after the same heparin dosage. The residual lactescence after post-heparin lipolysis was associated with no significant deviation of coronary dynamics from the normal. That a concentration-dependent phenomenon is operative, was confirmed in a separate group of patients in whom low lactescence values developed in the course of alimentary lipemia without affecting myocardial oxygen consumption. The relevance of the lipemic state, per se, to the pathophysiology of myocardial ischemia appears to depend upon the establishment of an oxygen gradient within the myocardium, presumably through altered pressure-flow relationships produced by lipemic blood within a pathologic vessel.

MYOCARDIAL TRANSFER OF SODIUM AND POTASSIUM: EFFECT OF ACETYL STROPHANTHIDIN IN NORMAL DOGS

Although the hemodynamic events attending low-output congestive heart failure have been well defined, the biochemical changes in the myocardium responsible for these events and the response to cardiac glycosides remain largely unknown. Evidence to date suggests that in the failing heart there is normal substrate oxidation but an impairment of energy utilization (1). Recent data would indicate an altered state of the myocardial protein-complex, actomyosin (2), but whether this is the primary event in the evolution of congestive failure remains to be demonstrated. Post-mortem tissue analyses for cation content of human heart muscle in failure have shown a lowered content of potassium (3, 4). Moreover, after digitalis, in therapeutic (5) and toxic doses (5, 6), the potassium content diminishes, although some disagreement over the former exists. That these changes may have functional significance is suggested by the work of Hajdu (7), who, from data obtained with a frog heart-muscle preparation, has inferred that the positive inotropism of digitalis is effected by the reduction in internal ionic content produced by the transfer of potassium from the cell. The pronounced effect of digitalis on the mechanical efficiency of the failing myocardium (8, 9) suggests that this drug might provide data re-

Left Ventricular Oxygen Consumption, Blood Flow, and Performance in Mitral Stenosis

The restriction imposed by mitral stenosis on the cardiac output response to exercise provides a unique opportunity in man to evaluate determinants of coronary flow and myocardial oxygen consumption, since one or several variables may be limited. Coronary and systemic hemodynamic patterns were therefore evaluated in 12 patients with mitral stenosis and compared with normal subjects.While cardiac output and left ventricular work were lower than normal at rest, coronary flow and myocardial oxygen consumption did not differ from normal. During exercise, despite subnormal cardiac output and left ventricular work responses, coronary blood flow and myocardial oxygen consumption increased normally in the group of patients in whom arterial pressure rose. However, coronary flow fell in four patients who experienced exertional hypotension, while myocardial oxygen consumption was reduced or unchanged. In both groups, myocardial oxygen extraction was above normal at rest and rose further during exercise. Changes in myocardial oxygen consumption followed alterations in the pressure-time index, but the excessive heart rate response to exercise resulted in a greater oxygen expenditure per unit of tension developed per beat than that found in normal subjects.It is concluded that the primary determinant of coronary blood flow in mitral stenosis is the arterial perfusion pressure while myocardial oxygen consumption is primarily dependent on the pressure-time index. In addition, heart rates inappropriately high for a given state result in energy expenditures above that required for maintenance of pressure and cardiac output.

Depression of Cardiac Function and Altered Myocardial Metabolism After Ethanol.

Excerpt In view of the ill-defined status of cardiac involvement in chronic alcoholism, a study of the acute effects of ethanol on myocardial metabolism and function has been undertaken in animals ...

Regression of intercoronary collateral vessels in mongrel dogs after coronary bypass grafting

Abstract Four dogs underwent direct revascularization of a chronically occluded circumflex artery with an internal mammary artery bypass graft. Preoperative coronary cineangiograms demonstrated well developed intercoronary collateral vessels supplying the circumflex arterial bed. Intraoperative measurements of retrograde circumflex arterial flow and pressure were consistent with the presence of large collateral vessels. Closed chest postoperative estimates of the potential collateral circulation were obtained by advancing a Judkins catheter to the internal mammary wedge position. The graft wedge pressure was equated to the retrograde circumflex pressure. After coronary bypass grafting, the interval coronary angiographic and hemodynamic studies indicated that well developed collateral vessels regressed within the first postoperative month to capacities in the range of those found in normal dogs.

Myocardial Blood Flow and Oxygen Uptake During Acute Red Cell Volume Increments

The role of red cell mass in the regulation of coronary blood flow and myocardial oxygen consumption has been examined after acute transfusion of sedimented red cells. Patients with substantial blood-loss anemia had a lower than normal left ventricular oxygen uptake, despite a high myocardial blood flow at rest. A 50% rise of hematocrit reduced coronary flow markedly. Although systemic arterial pressure, cardiac output, and left heart work rose, myocardial oxygen consumption was unchanged. Red cell transfusion of normovolemic dogs resulted in a decrease of both myocardial flow and oxygen uptake associated with an elevation of time-tension index and left ventricular work, accelerated isometric contraction and prolonged systole. There was no evidence of ischemia or change of left ventricular hemodynamic parameters that would account for the reduced myocardial blood flow and oxygen uptake. These findings, in the presence of an increased oxygen carrying capacity and extraction, would appear to be related principally to enhanced blood viscosity.

Studies in a cardiovascular model on the arterial dilution curve of valvular regurgitation

Abstract Many methods for assessing valvular regurgitation, including techniques which attempt to quantify backward flow, are based on analysis of deformities characteristically observed in arterial dilution curves. The present study was designed to ascertain what these methods actually measure. Dye was injected into the atrium, and dilution curves were recorded continuously from the elastic aorta of a pulsating two-chambered cardiovascular model. Forward flow, backflow, ventricular stroke and end-systolic volumes, and atrial size, shape, and elasticity were systematically varied. One hundred and seventeen experiments were performed. In 61 experiments the atrioventricular valve was made incompetent, with backward flows ranging from 8 to 73 per cent of total ventricular output. With forward flow and central volume held constant, enhancement of mixing, produced by altering atrial geometry or the distribution of fluid between atrium and ventricle, reproduced the earlier appearance, lower peak, flatter downslope, and wider spread seen with valvular regurgitation. Qualitatively and quantitatively indistinguishable dilution curves were produced in the presence and absence of regurgitation by appropriate manipulation of mixing. For a given forward flow, with or without regurgitation, the spread of dilution curves was related to Newmans mixing volume by a single regression line, but to Hamiltons central volume by a family of such lines, each uniquely determined by the ratio of mixing volume to central volume. With forward flow and mixing volume held constant, the dilution curve was unaltered by the introduction of valvular regurgitation. These results demonstrate the following: (1) The parameters of dilution curves obtained downstream to a valve, after injection upstream, are functions of forward flow and of a volume, real or virtual, in which indicator has effectively mixed, whether or not valvular regurgitation is present. (2) Methods which assess valvular regurgitation by analysis of such curves do not measure regurgitant flow. They are merely indices of an enhanced mixing which usually, but not inevitably, accompanies regurgitation.