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Biomedical subjects

D A Ehrich

Publications and source records attributed to D A Ehrich.

10 recordsLinked to original sources
PubMed1994

Response of patients with coronary artery disease stratified by ejection fraction following short-term training.

The purpose of this study was to investigate the response of patients with ischemic heart disease and varied left ventricular function following 6 weeks of exercise training. We studied the oxygen consumption (VO2), and central hemodynamic and metabolic responses of 14 patients with coronary artery disease (CAD) stratified by left ventricular ejection fraction (EF). There were two groups of patients: normal EF (NEF), EF = 64 +/- 9.9 (mean +/- S.E.M.); n = 7, and diminished EF (DEF), EF = 36 +/- 11.6; n = 7. The patients ranged in age from 42 to 72 years (54.9 +/- 2.2), and were evaluated prior to and then following training. Measures of VO2, cardiac output (Qt) stroke volume (SV), heart rate (HR), exercise duration (XTIME) and intensity (XI), as well as plasma lactate (LA), and the catecholamines epinephrine (E) and norepinephrine (NE) were obtained in response to maximal cycle ergometry. Subjects trained three times per week, 30 min per session, at an intensity equal to 70% of their peak oxygen consumption. Repeated measures analysis of variance (ANOVA) revealed no interaction between groups suggesting a similar training response. Significant post-training changes (P < 0.05) were observed in peak VO2 (VO2peak) NEF, 11.8% increase, (16.0 +/- 1.3 to 17.9 +/- 1.1 ml/kg/min) and DEF, 9.3% increase (15.1 +/- 1.6 to 16.5 +/- 1.2 ml/kg/min); submaximal HR, 4% decrease in the NEF (95.57 +/- 4.58 to 92 +/- 4.43 beats/min) and a 6% decrease in the DEF (107.29 +/- 7.44 to 101.43 +/- 6.77 beats/min); XTIME NEF, 11.2% increase (7.8 +/- 0.57 to 8.67 +/- 0.61 min) and DEF, 16.6% increase (7.3 +/- 0.91 to 8.51 +/- 0.69 min); and XI NEF, 19.2% increase (104.3 +/- 11.3 to 124.3 +/- 12.9 W) DEF, 21.2% increase (94.3 +/- 18.5 to 114.3 +/- 16.9 W), and a 15% decrease in resting NE (350 +/- 26 to 296.9 +/- 19 pg/ml). There were no changes in Qt, SV, LA, E, peak NE or peak HR for either group. These findings suggest short-term endurance training at 70% VO2peak provide the necessary stimulus for individuals with CAD and NEF or DEF to display an improvement in XI, XTIME, and VO2peak. The lack of a significant enhancement in Qt with short-term training may indicate that the mechanism by which both study groups were able to attain significantly higher levels of VO2peak may have been attributable to peripheral mechanisms rather than any alterations in Qt, a central mechanism.

Coronary Disease↗
PubMed1977

The hemodynamic response to intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction.

Sixteen patients with cardiogenic shock complicating acute myocardial infarction underwent serial hemodynamic studies during intra-aortic balloon counterpulsation (IABC) at an assist frequency of 1:1. Significant increase was noted during the first 12 hours of IABC in the systemic artery peak diastolic pressure (assisted), cardiac index, stroke index, and stroke work index. During the second 12 hours further significant improvement was noted in the latter three parameters and, in addition, the systemic artery systolic pressure increased significantly. The pulmonary wedge pressure fell as did the total systemic resistance (TSR) during the first 24 hours of IABC. Patients found to be balloon independent after reduction in balloon assist frequency demonstrated significantly greater increase in systemic artery peak diastolic pressure during the first 12 hours of IABC than did those patients found to be balloon dependent. Likewise, the improvement noted in CI, SI, and SWI during the second 12 hours of IABC was of greater magnitude in balloon-independent than in balloon-dependent patients. The data suggest late hemodynamic deterioration after 48 hours of IABC. It is concluded that IABC is effective in improving the deranged hemodynamics of cardiogenic shock. Maximum response is noted between 24 and 48 hours. It is suggested that patients who are balloon independent may be distinguished from those who are balloon dependent by the hemodynamic response within the first 24 hours of IABC.

Acute Disease↗
PubMed1976

Hypoxemia and lung water in acute myocardial infarction.

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.

Adult↗
PubMed1976

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

The degree of vectorcardiographic ST-segment 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 muV (mean +/- SE). A standard deviation of the pooled variance of 15.2 muV was obtained in a group of control patients and a change of more than 2 SD (greater than 30 muV) 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 muV 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 muV 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 extopy but also lethal conduction abnormalities after AMI might be ischemia-related.

Acute Disease↗
PubMed1975

Intracavitary cardiac extension of hepatoma.

Acute right atrial obstruction in a 62-year-old man was demonstrated angiographically to be due to a tumor, which was later proved to be metastatic hepatoma. Resection of the tumor resulted in total symptomatic relief.

Bile↗