Gerald W. Murphy

Cardiac output in acute myocardial infarction: Serial determination by precordial radioisotope dilution curves☆

Abstract Serial determinations of cardiac output were performed in 16 patients with acute myocardial infarction, utilizing precordial detection of indicator-dilution curves following an intravenous injection of radioiodinated human serum albumin. The evolution of hemodynamic events in these patients is documented, and the clinical data are correlated with concurrent circulatory findings. Results indicate that: (1) Persistently low cardiac index and stroke index were found only in fatal cases. (2) Survivors either maintained a normal cardiac index and stroke index or, if initially observed as abnormal, values for these two parameters generally returned to normal during recovery. (3) Low stroke index was the commonest basic hemodynamic abnormality. Normal values for stroke index were not found in the fatal cases. (4) Ventricular gallop rhythm and tachycardia were found to be reliable clinical guides to the presence of low stroke index. (5) Pulse pressure values were not a useful clinical measure of stroke index.

Hemodynamic studies of the portal circulation in myeloid metaplasia

P ORTAL hypertension occasionally has been described in association with several hematologic diseases [P-70]. In some cases an extrahepatic venous obstruction has been demonstrated [7,9], in other instances intrahepatic obstruction of the portal system has been the apparent etiology [ 7,3]. In a few reported cases, despite clear evidence of portal hypertension, no evidence of either intraor extrahepatic anatomic obstruction to portal blood flow was apparent [4-61. Several investigators have directed attention to indications of portal hypertension in patients with myeloid metaplasia. Hunt [IO] studied a patient with this disorder and documented significant portal hypertension, which was corrected by splenectomy. Another such patient with myeloid metaplasia and hemorrhage from bleeding esophageal varices was studied by Shaldon and Sherlock [7], and found to have presinusoidal obstruction of the portal venous system. In a recently reported series of cases, esophageal varices were found in two of eighteen autopsy patients and one of these had no obvious block [5]. In addition, reference has been made to “unexplained” ascites and edema in patients with myeloid metaplasia 161. Among the twentynine patients described by Nakai, Craddock and Figueroa [6], seven had edema and three ascites. Two of the three patients with ascites were studied at autopsy, and no obvious portal block was identified. A patient with myeloid metaplasia, portal hypertension and bleeding esophageal varices was studied in this clinic in 1960 [4]. Neither intrahepatic nor extrahepatic obstruction could be demonstrated. This patient underwent a successful end-to-side portacaval shunt and survived for an additional two years, although her course was complicated by the development of mild recurrent hepatic encephalopathy. These workers postulated that the portal hypertension in this instance was of a hyperdynamic type, caused by augmented blood flow through the massively enlarged spleen and into the portal system. The results of studies of portal and systemic hemodynamics in five patients with myeloid metaplasia, several of whom exhibited esophageal varices, and/or edema and ascites, are reported herein. One case is described in detail, with autopsy findings; the others are presented briefly.

Surgical Treatment of Traumatic Rupture of the Normal Aortic Valve

Abstract The histories of 2 patients who had successful repair of traumatic injury to the aortic valve are reported, and the literature is reviewed. Various types of injury cause this lesion, but violent compression of the chest with high intrathoracic pressure appears to be a common feature. Valvular injuries include avulsion of commissural attachments and tears of the leaflets. Patients present with chest pain and severe congestive heart failure, and an unusually musical murmur of aortic insufficiency is sometimes heard. Attempts at valvuloplasty have not been uniformly successful, and prosthetic valve replacement is recommended.

Acute electrocardiographic pseudoinfarction pattern in the setting of diabetic ketoacidosis and severe hyperkalemia

aVF was observed during the procedure. No complications were encountered during and after procedure. Corticosteroid therapy 10 to 30 rag/day (prednisone for 6 months) was begun, with resultant normalization of the erythrocyte sedimentation rate. Follow-up treadmill testing 2 months after the procedure revealed electrocardiographic changes during moderate exercise (Bruce stage 5, 50 mph at a grade of 18%) and associated significant ST segment depressio n of 2 to 4 mm in leads II, III, aVF, and V2 to V6. Follow-up coronary angiography 27 months after the PTCA revealed no evidence ofrestenosis of the left coronary artery (Fig. 1, C). The post-PTCA clinical course was uncomplicated, and the patient has had no symptoms over a 2-year period after balloon angioplasty. Recently, balloon angioplasty of the aorta in Takayasus arteritis has produced good results both immediately after the procedure and on long-term follow up. 4 No aneurysm at the site of angioplasty was found in these patients. Markedly thickened vessel wall resulting from inflammatory fibrosis of all three layers as observed in Takayasus arteritis could reduce the risk of future aneurysm formation. 5 To our knowledge this is the first case of PTCA for coronary artery stenosis in Takayasus arteritis. Hitherto, PTCA in Kawasaki disease has been reported. One patient with Kawasaki disease who had undergone PTCA for coronary artery stenosis died of obstruction of the left coronary artery immediately after balloon rupture caused by a high inflating pressure occurred. Two other patients underwent successful dilation. 6, 7 Acute obstruction is an inherent risk of PTCA and can be deleterious in left coronary artery main stem lesions. However, recent results of aortocoronary bypass grafting have not been satisfactory. Ohara et al. s reported a low graft patency rate (50%) in their six patients undergoing aortoc0ronary bypass grafting. Cippiano et al.9 stated that it was difficult to construct proximal anastomoses of the grafts because of extremely thickened aortic wall, and inflammation of the aortic wall may have contributed to the late proximal occlusion of bypass grafts. This case suggests that PTCA may well be an effective alternative method to aortocoronary bypass surgery for coronary artery stenosis in Takayasus arteritis. REFERENCES

Pulmonary Blood Volume in Congestive Heart Failure

By utilizing indicator-dilution techniques, determinations of the pulmonary blood volume (PBV) and central blood volume (CBV) were made in 25 patients during simultaneous right and transseptal left heart catheterization. Of these, 12 patients had normal hemodynamics, six had heart failure associated with mitral stenosis, and seven had heart failure secondary to nonvalvular myocardial disease.In the normal patients the PBV averaged 271 ml/m2 (SE, ±10.0) and the CBV 596 ml/m2 (SE, ±25.7). The mean value for PBV and CBV in the patients with heart failure associated with mitral stenosis was 238 ml/m2 (SE, ±26.3) and 600 ml/m2 (SE, ±40.9), respectively. Among the patients with nonvalvular heart failure the PBV averaged 292 ml/m2 (SE, ±21.4) while the CBV averaged 679 ml/m2 (SE, ±45.8). In 12 of the 13 patients with heart failure, the individual values for PBV and CBV did not differ significantly from normal. However, in each of the 13 patients pulmonary artery, left atrial, and mean pulmonary distending pressures were significantly elevated, whereas the relative pulmonary vascular compliance was greatly reduced.These findings indicate that the pressurevolume relationships within the pulmonary vascular bed are greatly altered in the presence of chronic pulmonary venous hypertension. Normal values for PBV were associated with significant pressure elevations in the presence of pulmonary congestion and edema.It is concluded that in the pathogenesis of heart failure elevations in pulmonary vascular pressures play a dominant role while changes in PBV are of but secondary importance. These findings do not support many of the traditional concepts regarding the role of pulmonary blood volume changes in the pathophysiology of heart failure.

Effect of Exercise on the Pulmonary Blood Volume in Patients with Acquired Heart Disease

The effect of supine exercise on the pulmonary blood volume was studied in 14 patients with valvular heart disease and in one patient with cardiomyopathy. Statistically significant increases occurred in the pulmonary blood volume (88.6 ± S.E. 20.9 ml./M.2) and in the central blood volume (121.9 ± S.E. 29.2 ml./M.2), whereas left atrial to brachial arterial volume remained unchanged. These results support the concept that, with exercise, increases in central blood volume reflect increases in pulmonary blood volume in patients with acquired heart disease. The increase in pulmonary blood volume and in pulmonary distending pressure suggests a passive expansion of the pulmonary vascular bed with exercise.

Angiocardiographic evaluation of mitral valve stenosis. Use in selection of surgical approach.

Some divergence of opinion exists as to the merits of “closed” versus “open” commissurotomy for the correction of pure acquired mitral stenosis (9). Part of this controversy is probably due to the small but real percentage of early failures, as well as to the relatively frequent recurrence of mitral stenosis following the procedure (6). Such recurrences and failures may be due in part to the presence of one of the following pathologic features of the mitral valve: insufficient closure; heavy calcification; significant reduction in functioning valve tissue with scarring and fusion; extensive deformities of the valve secondary to abnormalities of the chordae tendineae. Also, thrombi in the left atrium, with their possible dislodgment at surgery, may present formidable technical problems for the surgeon. The assessment of the functional derangement of the mitral valve is best achieved by selective angiocardiography, in conjunction with and complementary to hemodynamic evaluations of cardiac function by simul...

Effects of Acute Digitalization on the Pulmonary Blood Volume in Patients with Heart Disease

Basic hemodynamic data and the pulmonary blood volume (PBV) were determined in 23 patients before and after intravenous administration of acetyl strophanthidin during right and left heart catheterization. These patients were divided into two groups depending upon whether or not digitalization produced a significant fall in left ventricular end-diastolic pressure (LVD). Group I consisted of 11 patients who manifested a significant decrease in LVD, while in group II no change was noted after digitalization. In both groups, a significant rise in LV stroke volume, stroke work, and maximal rate of rise of LV systolic pressure (dp/dt) was recorded. In group I, a significant decrease in the pulmonary vascular distending pressure (Pd) was accompanied by a decrease in PBV. In contrast, no change in Pd or PBV was noted in the patients in group II. Changes in pulmonary vascular resistance (PVR) were inconsistent. It is concluded that: (1) in patients of group I the concordant decrease in Pd and PBV represented a passive effect on the pulmonary vascular bed mediated by improved LV performance and decrease in LVD; (2) in patients of group II, despite evidence of significant positive inotropic effects on the left ventricle, the failure of LVD to fall prevented a decrease in Pd and PBV; (3) no evidence of active vasomotor effects of acetyl strophanthidin in the lung could be demonstrated. Changes in PVR were capricious and not apparently useful in assessment of the presence or absence of pulmonary vasomotor effects induced by digitalis. The results of this study differ from the findings of other investigators in cardiac patients and experimental animals. Some of the differences may be attributed to different experimental methods and to species variation in vascular reactivity.Also, the findings in this report contrast with those previously reported for isoproterenol and aminophylline, agents that produce both positive inotropic effects on the heart and active vasomotion in the pulmonary circulation.