Search PubMed⌕ Search

Biomedical subjects

R Grose

Publications and source records attributed to R Grose.

27 records · Page 2Linked to original sources

Left ventricular volume and function during relief of cardiac tamponade in man.

To determine the causes of cardiac failure during cardiac tamponade in man, we studied left ventricular volume and function in eight patients during pericardiocentesis using gated equilibrium radionuclide ventriculography. In the seven patients with clinical and hemodynamic evidence of cardiac tamponade, end-diastolic and end-systolic volumes increased progressively as the initial 500 ml of fluid were removed; the most marked increase occurred during the removal of the first 200 ml of pericardial fluid. After removal of 500 ml of pericardial fluid, end-diastolic volume increased from 52 +/- 8 ml to 111 +/- 13 ml (p less than 0.05) and end-systolic volume from 17 +/- 5 ml to 34 +/- 7 ml (p less than 0.05). Additional aspiration of fluid resulted in no further changes in left ventricular volume. The ejection fraction averaged 70% before removal of fluid and was unchanged by pericardiocentesis. In the one patient who did not have hemodynamic evidence of tamponade, there were only minor changes in left ventricular volumes and ejection fraction. These data suggest that pump function of the left ventricle is well preserved in cardiac tamponade, and that the diminution in stroke volume and consequent cardiovascular collapse seen in tamponade are due to marked underfilling of the ventricle.

Cardiac Output↗

Recognition of bicuspid aortic valve by plain film calcification.

Differentiation of bicuspid aortic valve from other causes of calcific aortic stenosis is not possible by echocardiography or, in many cases, by aortography. This report describes newly recognized patterns of calcification on plain films that are diagnostic for a bicuspid aortic valve. These are based on identification of the calcified raphe and/or the calcified conjoint leaflet. In 120 patients who underwent surgical repair of calcific aortic stenosis, 40 were found to have bicuspid valve. Examination of the plain films retrospectively allowed a correct recognition of 26 (65%) of these valves. In contrast, only 10 (25%) could be recognized by aortography. Patterns of calcification on plain films represent an important tool for detection of calcified cogenital bicuspid aortic valve.

Aortic Valve↗

Right ventricular dysfunction in acute ventricular septal defect.

Eight patients with acute ventricular septal defect (VSD) receiving early intra-aortic balloon augmentation, cardiac catheterization, and open-heart surgery are described. Because of the large shunts in this group of patients, there was visualization of the right ventricle during left ventriculography which was adequate for qualitative analysis. The following were noted: (1) All patients had severe right ventricular (RV) dysfunction angiographically. (2) RV akinesis noted on angiography was more extensive than the surgical description of RV infarction, although all patients had biventricular infarction at surgery. (3) The RV dysfunction was the major cause of death (two cases) or a contributing factor (three cases). (4) RV papillary muscle rupture was identified in one case.

Acute Disease↗

Production of left ventricular cavitary obliteration in normal man.

To determine whether left ventricular cavitary obliteration (a finding previously described only in hypertrophic states) can be induced in normal subjects, 16 patients without coronary artery disease or clinical evidence of hypertrophic obstructive cardiomyopathy were studied during cardiac catheterization. Resting left ventricular and aortic pressures and left ventriculography were repeated during the strain phase of Valsalva maneuver after administration of amyl nitrite. Cavitary obliteration during normal sinus rhythm was defined as disappearance of the sinus portion of the left ventricle during systole, and graded as absent, partial or total. Patients were placed into two groups on the basis of qualitative analysis of the resting left ventriculogram: the 10 patients in group A had normal left ventriculograms and the six patients in group B had hyperkinetic left ventricles. During the left ventriculogram done with amyl nitrite and Valsalva, left ventricular volumes in both decreased dramatically, from 69 ml/m2 to 43 ml/m2 (p less than 0.001) and ejection fraction increased from 70% to 82% in group A (p less than 0.01). None of the patients in group A had evidence of cavitary obliteration at rest, but eight developed total and two developed partial cavitary obliteration with the second ventriculogram. Three patients in group B had partial or complete cavitary emptying at rest and all developed total cavitary obliteration with provocation. Pressure gradients between left ventricle and aorta were produced in two group A patients and three group B patients. Thus, cavitary obliteration can be produced in normal left ventricles by manipulation of loading conditions.

Adult↗

Clinical and hemodynamic correlation in patients with pericardial effusion and swinging heart by echocardiography.

The clinical and hemodynamic findings in 13 consecutive patients with "swinging heart" on M-mode echocardiography were analyzed. In these patients the anterior right ventricular and posterior left ventricular walls and interventricular septum moved almost parallel to each other throughout the cardiac cycle, often with exaggerated excursion. In 10 of 13 patients right heart catheterization revealed the hemodynamic profile of cardiac tamponade, while one additional patient was found to have evidence of cardiac compression at the time of surgery. In the remaining two patients no acute invasive diagnostic procedures were performed. During the same observation period cardiac tamponade was observed in five patients without echocardiographic evidence of a swinging heart, and four of these had large clots in the pericardial space. Thus, the swinging heart pattern appears to be a reliable marker of cardiac tamponade, except in those patients with intrapericardial lesions which mechanically limit cardiac motion.

Adult↗

Cardiac tamponade in dogs with normal coronary arteries. I. Effect of changing intravascular volume on hemodynamics and myocardial blood flow.

Intravascular volume expansion has been shown to improve cardiac output in experimental cardiac tamponade. To determine the limitations of intravascular volume manipulation, acute tamponade was created in 20 anesthetized, spontaneously breathing dogs. The intrapericardial volume causing tamponade was determined for each animal, and kept constant. Hemodynamics were recorded with and without tamponade at multiple levels of intravascular volume. During cardiac tamponade, intravascular volume expansion increased cardiac output only in animals which were initially volume-depleted. Volume expansion of normovolemic or hypervolemic animals caused minimal changes in cardiac output, but increased atrial and aortic pressures. Intravascular volume depletion of the normovolemic animal caused a significant decline in cardiac output, in contrast to the trend towards an increased output following phlebotomy of the volume-expanded animals. In general, the benefit of intravascular volume expansion during cardiac tamponade could only be demonstrated when atrial pressures were below 12 mm Hg.

Animals↗

Cardiac tamponade in dogs with normal coronary arteries. II. Myocardial flow and metabolism with moderate and severe hemodynamic impairment.

To determine the effects of cardiac tamponade on myocardial blood flow and its distribution, dogs were prepared with indwelling pericardial catheters. Hemodynamic, myocardial blood flow, and myocardial metabolic data were collected in 5 closed-chest, spontaneously breathing animals with normal blood volumes and hemoglobin concentrations and 6 with acute anemia. Instillation of an average of 89.0 +/- 14.9 ml of modified Normosol into the pericardial space in dogs with normal hemoglobin levels produced mild tamponade with a modest decline in aortic pressure (119.5 +/- 14.3 to 96.8 +/- 12.1 mm Hg) and significant rises in left and right atrial and pericardial pressures to 7-8 mm Hg. Increasing the pericardial volume to 124.0 +/- 13.6 ml produced hypotension (mean aortic pressure 86.2 +/- 10.5 mm Hg) and rises in the left and right ventricular filling pressures and pericardial pressure to 10-11 mm Hg. Total myocardial blood flow fell from 1.19 +/- 0.18 to 0.73 +/- 0.17 ml/min/g (p less than 0.02) during mild tamponade, and fell further to 0.56 +/- 0.17 ml/min/g (p less than 0.05) with more severe tamponade. Despite these declines, the left ventricular wall inner/outer flow ratio and left ventricular flow as a proportion of total cardiac output were unchanged. In dogs with anemia more severe tamponade was created, with consequently more marked hemodynamic abnormalities. However, the relative changes in myocardial blood flow and inner/outer flow ratio were similar. Myocardial metabolic parameters could be evaluated only in the dogs with less severe tamponade.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Gastric mucosal bleeding time in cirrhosis.

Gastric mucosal bleeding time was measured prospectively in 25 patients with cirrhosis and portal hypertension undergoing routine sclerotherapy. Age and sex-matched controls without liver disease were also studied. Correlations were sought between gastric mucosal bleeding time and age, platelet count, prothrombin time, skin bleeding time, Child-Pugh score, variceal size before sclerotherapy, and degree of portal hypertensive gastropathy. Gastric bleeding time was prolonged in 12% of the patients with cirrhosis (mean, 3.24 minutes; SEM, 0.476) and in none of the controls (mean, 3.0; SEM, 0.171). No correlation was noted between gastric bleeding time and any of the above variables. The results of this study indicate that gastric mucosal bleeding time is prolonged in cirrhosis but is an independent physiologic parameter unrelated to any of the above-mentioned variables.

Bleeding Time↗