Paul N. Yu

Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction

Hemodynamic studies were carried out in 19 patients with left ventricular failure complicating acute myocardial infarction. Fourteen patients were studied before and after the intravenous administration of 0.5 mg/kg of furosemide, and five patients served as a control group. Serial measurements included intracardiac pressures, cardiac output and lung water by a double isotope technique. A significant reduction was noted in right atrial (P less than 0.005), pulmonary arterial (P less than 0.0005) and pulmonary wedge pressures (P less than 0.0005) after administration of furosemide. Only the change in right atrial pressure was significantly different from that in the control group (P less than 0.05). Lung water was not changed in 4 patients studied 2 hours after administration of furosemide but was significantly changed in the remaining 10 patients studied 4 to 24 hours after furosemide (P = 0.0001). This change was also significantly different from values in the control group (P less than 0.05). The patients with no reduction in excess lung water also had a smaller reduction in pulmonary wedge pressure and a lower pretreatment stroke work index than the other patients. The mobilization of excess lung water in patients with acute myocardial infarction complicated by left ventricular failure has several features. Despite a prompt diuresis, the reduction in lung water is delayed for at least several hours after the administration of furosemide and may be related to the degree of left ventricular dysfunction. Venodilation may be a major result of treatment with furosemide.

Hemodynamic and respiratory effects of morphine and butorphanol.

The hemodynamic effects of butorphanol, a potent synthetic narcotic‐antagonist analgesic, were investigated and compared with those of morphine. A total of 20 patients were studied (8 butorphanol, 12 morphine) at the time of diagnostic cardiac catheterization. Butorphanol decreased pH, PCO2, and systemic artery pressure and increased PCO2, cardiac index, and pulmonary artery pressure. Morphine caused similar changes in pH, PO2, systemic artery pressure, and PCO2 but much smaller changes in cardiac index and no change in pulmonary artery pressure. The clinical implications and possible mechanisms are discussed.

Pulmonary function during pregnancy in normal women and in patients with cardiopulmonary disease

Pulmonary function studies were carried out during pregnancy in 8 normal women, in 8 patients with valvular (either mitral or aortic) heart disease, and in 8 patients with chronic pulmonary disease (either emphysema or sarcoidosis). In healthy pregnant women, changes in lung volumes and maximal expiratory flow rates were not significant. Diffusing capacity tended to decrease associated with unchanged pulmonary capillary blood volume. In patients with valvular heart disease, ventilation and oxygen consumption increased toward the term. The patients with mitral valve lesions showed a significant decrease in diffusing capacity with an increase in pulmonary capillary blood volume. In patients wth emphysema, characteristic changes were increasing obstructive functional abnormalities associated with an increase in pulmonary diffusing capacity and pulmonary capillary blood volume. None of these patients, however, had clinical evidence of deterioration of their disease. Patients with sarcoidosis had no appreciable alteration in pulmonary function tests. The influence of various factors, such as increased ovarian hormones, ventilation-perfusion relationships, intra-abdominal distension, and cardiac haemodynamics, are discussed in relation to the change in pulmonary diffusing capacity and pulmonary capillary blood volume. From the standpoint of pulmonary function studies we think that patients with mitral heart disease and those with pulmonary emphysema tolerate pregnancy less favourably than normal subjects and patients with sarcoidosis.

Pulmonary Function in Idiopathic Scoliosis

Pulmonary function studies were reported in sixty-two patients with idiopathic scoliosis with ages ranging between ten and twenty years and were compared with the data obtained from fifty-three normal subjects of a similar age group. Twenty-Six of the normal subjects were siblings of the patients.nnAbnormalities in pulmonary function were noted in twenty-nine patients. There was a predominant restrictive type of respiratory abnormality in fourteen, a reduction in pulmonary diffusing capacity in twelve, and a decrease in expiratory flow rates in three. The most common physiological abnormality was a decrease in lung volumes, particularly in vital capacity and its components. Decrease in pulmonary diffusing capacity was usually associated with reduced lung volumes. Pulmonary capillary blood volume was normal in all patients.nnOne to four years after corrective surgery, follow-up pulmonary function evaluation was repeated in thirty-three patients. In these patients, the average precorrection spinal curve was 62 degrees, and the average final curve after correction and stabilization was 21 degrees. In the postoperative period, improvement of pulmonary function toward normal was observed in twelve patients. Sixteen of thirty-three patients had normal pulmonary function before and after surgical treatment, suggesting that they would have a better chance for their pulmonary status to remain normal in the future because of correction of their spinal curves.

Left Ventricular Performance Following Digitalization in Patients with and without Heart Failure

Nine patients, three with left ventricular failure and six with compensated heart disease, were studied by means of right and transseptal left heart catheterization duringacute digitalization with acetyl strophanthidin. One of the patients with heart failure and a compensated subject with the Wolff-Parkinson-White syndrome were also studied during supine left leg exercise.In the decompensated group, digitalization produced a decrease in heart rate and increases in stroke index, stroke work, mean stroke power, mean systolic ejection rate, and the rate of pressure rise in the left ventricle. Left ventricular end-diastolic pressures were markedly lowered after digitalization.In the compensated group, no significant changes in cardiac index, stroke index, or mean systolic ejection rate were observed. Although there were small increases in stroke work and power and moderate decreases in left ventricular diastolic pressures, the most striking finding was an increase in the rate of rise of left ventricular systolic pressure.Digitalization produced considerable improvement in the circulatory response to light exercise in a patient with left ventricular failure. Less marked improvement in the exercise response was observed in a patient with normal hemodynamics. After digitalization, left ventricular function points plotted on the stroke work end-diastolic pressure diagram tended to shift upward and to the left in both decompensated and compensated patients. The shift of function points was most prominent in the decompensated group.This study demonstrates that, in the presence of myocardial failure, acetyl strophanthidin markedly augments left ventricular performance. Furthermore, the data suggest that digitalization also improves left ventricular performance in patients with left ventricular enlargement but no clinical manifestations of heart failure.

Distensibility Characteristics of the Human Pulmonary Vascular Bed: Study of the Pressure-Volume Response to Exercise in Patients with and without Heart Disease

The changes in pulmonary blood flow, pressure, and volume during supine exercise are studied in seven patients without cardiovascular abnormality, 12 patients with aortic valve disease, 13 patients with mitral valve disease, and five patients with primary myocardial or pericardial disease. The degree of distensibility of the pulmonary vascular bed is assessed by the simultaneous changes in the magnitude of the pulmonary distending pressure (average of pulmonary artery and left atrial pressure) and of the pulmonary blood volume.

The acute hemodynamic effects of ethacrynic acid and furosemide in patients with chronic postcapillary pulmonary hypertension.

The acute hemodynamic effects of either ethacrynic acid or furosemide were studied in 27 patients who underwent diagnostic right and transseptal left heart catheterization. Twentythree patients had postcapillary pulmonary hypertension secondary to isolated or predominant mitral stenosis. Of these, 21 patients were in New York Heart Association functional class 111, and one each in class II and IV. In the remaining four patients pulmonary artery pressures were normal. Two patients had aortic stenosis and one each coronary artery disease and nonobstructive cardiomyopathy. All four patients were in class H. Cardiac index, pressures, and pulmonary blood volume (PBV) were measured in the control state and 20, 40, and 60 min after diuretic administration. Pulmonary extravascular fluid volume (PEV) was measured in the control state and at 60 min post drug infusion. A similar hemodynamic response was observed for each drug. Significant reductions in pulmonary artery and left atrial mean pressures, cardiac index, and plasma volume occurred over the one hour observation period and were accompanied by a significant diuresis. However, despite reductions in central pressures and blood flow, PBV, PEV, and PEV/PBV remained unchanged, as did systemic arterial pressure. Since 23 of the subjects had postcapillary pulmonary hypertension it is postulated that the failure of PBV to decrease significantly despite significant decreases in pulmonary artery mean pressure is related to altered pressure volume characteristics in the pulmonary vascular bed in which the lung is operating on a steep portion of its pressure volume curve. The failure of the PEV to decrease supports the concept that the pulmonary extravascular space is relatively resistant to early decreases in pulmonary capillary pressure induced acutely. The failure of the pulmonary extravascular fluid volume to decrease despite a fall in plasma volume and pressures corresponds to the well recognized delay in resolution of radiologic evidence of pulmonary congestion.

Effects of Aminophylline on the Pulmonary Circulation and Left Ventricular Performance in Patients with Valvular Heart Disease

The effects of aminophylline given intravenously on the pulmonary circulation and left ventricular performance were studied during combined right and transseptal left heart catheterization in 32 patients with mitral and aortic valvular disease. We recorded complete data on the changes of the pulmonary vascular distending pressure (PD) and the pulmonary blood volume (PBV) before and during aminophylline infusion in 28 patients. In 19 patients a fall in the PD was associated with a rise in the PBV. In eight patients a decline in the PD was accompanied by a fall (five patients) or no change (three patients) in the PBV. In a single case, both PD and the PBV rose. In the majority of cases, observation of decrease in PD and a discordant rise in PBV is new evidence suggestive of a direct active vasodilating effect of aminophylline on the pulmonary vasculature.Although the cardiac index was unaffected, a positive inotropic effect on the myocardium was documented by a decrease in left ventricular end-diastolic pressure accompanied by an increase in the maximum rate of ventricular pressure rise (LV dp/dt). These findings contrast with those in certain patients with heart failure of nonvalvular origin in whom increases in cardiac index are usually prominent. The salutory effect of aminophylline in acute pulmonary edema is thought to be due to synergistic effects on the systemic circulation, pulmonary circulation, and left ventricular function, all of which tend to produce a fall in PD.

ST-segment variations after acute myocardial infarction. Relationship to clinical status.

SUMMARY The degree of vectorcardiographic ST-sgment elevation was employed as an index of myocardial ischemic injury in a study of 27 patients after acute myocardial infarction (AMI). The ST-segment vector magnitude (STVM) was derived from the continuously recorded modified Frank vectorcardiogram and was plotted serially by hours after onset of AMI. The STVM in normal subjects was 51.1 ± 7.1 μV (mean ± SE). A standard deviation of the pooled variance of 15.2 1iV was obtained in a group of control patients and a change of more than 2 SD (> 30 μV) in an individual STVM was considered to be significant. The STVM progressively decreased in patients who survived without clinical complications while it remained elevated in those with congestive heart failure. A modest, sustained re-elevation of STVM was observed in patients who developed pericarditis, and a significant late average increase of 64 μV occurred in survivors with infarct extension. In contrast, STVM underwent a major increase in patients who died. In five of these six patients without associated pericarditis a mean increase of 164 μV was recorded in the last 5–12 hours of life. While death was clinically predictable in two patients with cardiogenic shock, it was not so for the four other patients who died. Thus, major increases in STVM frequently suggested significant new ischemic injury and were often premonitory to sudden death after AMI. The increases preceding death implied that not only ventricular ectopy but also lethal conduction abnormalities after AMI might be ischemia-related.

Lung Water in Patients with Acute Myocardial Infarction

Pulmonary extravascular water volume (PEV) or lung water was measured in 45 patients with acute myocardial infarction, utilizing the double radioisotope indicator dilution technique. A PEV greater than the upper limit or normal (120 ml/m2) was found in 27 patients, 23 of whom had an elevated pulmonary wedge or pulmonary artery diastolic pressure. A significant correlation was found between PEV and pulmonary wedge or pulmonary diastolic pressure in the whole series. A progressive increase in average PEV was observed from Class I (uncomplicated) to Class IV (shock) patients. There was also a progressive increase in PEV from patients with normal chest X-ray findings to those with radiologic evidence of acute pulmonary edema. In seven of 11 patients with initial elevation of both PEV and pulmonary wedge pressure, repeat determinations demonstrated a substantial reduction in both parameters over a period of 2-4 days.We postulate that an increased PEV in patients with acute myocardial infarction is largely due to an elevated pulmonary capillary pressure. The latter is probably a consequence of an elevated left ventricular diastolic pressure, which may be a manifestation of either left ventricular failure or a decrease in left ventricular compliance.