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Biomedical subjects

M Hodges

Publications and source records attributed to M Hodges.

At least 109 records · Page 6Linked to original sources
PubMed1979

Follow-up of 514 consecutive patients with cardiopulmonary arrest outside the hospital.

During the years 1974 of 1976, 514 patients with prehospital cardiopulmonary arrest were brought to the Hennepin County Medical Center (HCMC) Emergency Department. Of these, 344 patients (67%) were either dead on arrival or died in the emergency department despite efforts at resuscitation. The remaining 170 patients were admitted to the coronary care unit. Eighty-seven patients (51%) died in the coronary care unit, primarily from uncontrolled rhythm disturbances and/or cardiogenic shock. The remaining 83 patients (16% of the total group, 49% of those admitted to the hospital) were discharged alive from HCMC. In this group, 49 patients of the 83 long-term survivors were ambulatory with full mental function when discharged. The remaining 34 patients were trnasferred to chronic care facilities for medical treatment of on-going problems. Of the 49 ambulatory patients, satisfactory data for follow-up was obtained on 47. Their mortality rate was 15% in the first year and 50% in the second, primarily from sudden death syndrome.

Adolescent↗
PubMed1979

Alterations in lung volume and pulmonary function in relation to hemodynamic changes in acute myocardial infarction.

To characterize the changes in lung volumes after acute myocardial infarction (AMI), and the relationship of these changes to other alterations in lung function which correlate with the severity of pulmonary vascular congestion, we made measurements of pulmonary hemodynamics, lung volume, closing volume, frequency dependence of total pulmonary resistance to forced oscillation, and arterial PO2 in 18 subjects with AMI. The most consistent finding was reduced lung volume which correlated with the severity of pulmonary diastolic hypertension. Frequency dependence of resistance showed a small but significant correlation with pulmonary hemodynamics. Closing volume measurements by the resident gas method in nine subjects was not related to hemodynamics. Follow-up studies at the time of hospital discharge revealed a significant return toward normal for arterial PO2, all lung volumes, and total pulmonary resistance at 9 Hz. Based on measurements in healthy subjects, the reduced lung volume after AMI may explain the changes in resistance. In acute and follow-up studies the degree of lung volume reduction and the severity of hypoxemia were strongly correlated.

Acute Disease↗
PubMed1979

Two-dimensional echocardiographic demonstration of left atrial thrombi in patients with prosthetic mitral valves.

Although M-mode echocardiography (MME) is not a reliable method for detecting left atrial thrombi, recent reports suggest that two-dimensional echo (2DE) may be more effective than MME in identifying intracardiac thrombi. In three patients with prosthetic mitral valves who presented with either arterial embolization or prosthetic valvular dysfunction, 2DE demonstrated left atrial masses consistent with thrombi, while MME was either negative (two patients) or suspicious (one patient) for left atrial thrombus. Thrombi were documented by surgical or postmortem examination in all cases. Clear delineation of the atrial cavity and the margins of the masses, visualization on multiple echocardiographic views and comparison of serial examinations were helpful in identifying these masses as thrombi. In addition, the masses visualized had certain patterns of motion which seem unique and may allow characterization of atrial masses as thrombi.

Blood Coagulation↗
PubMed1976

Echocardiographic study of the effects of acute left atrial hypertension on left atrial size.

This study was designed to investigate the effects of acute left atrial hypertension on left atrial size. Twenty-four patients with acute myocardial infarction were studied. The estimated mean left atrial pressure (LAm) was correlated with left atrial (LA) size obtained by echocardiogrphy. The LAm was elevated (greater than 12 mmHg) in 15 patients (Group I). The LA size was within normal limits in all but two patients who had minor increases. The LAm was normal in nine patients (Group II). The LA size was normal in each case. The LA size remained unchanged in those patients who had a stable LAm. We conclude that acute increases in LAm are not usually associated with LA enlargement beyond the upper limit of the normal range.

Blood Pressure↗
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

Ventricular arrhythmias and cardiac hemodynamics in patients with myocardial infarction. Comparison of the acute and post-hospitalization phases.

Sixty-six patients with myocardial infarction (MI) were studied during the acute hospital phase and during the six months after hospital discharge. The clinical characteristics, location of infarction, and data from right heart catheterization were studied in an attempt to determine what factors were associated with ventricular rhythm disturbance. Those patients with serious ventricular arrhythmias (SVA) in the acute phase of infarction were found to have a significantly greater degree of myocardial dysfunction as measured by pulmonary artery and pulmonary wedge pressure than patients with more normal rhythm (p less than .05). Clinical classification of patients and location of infarction were not helpful in predicting SVA during the acute infarction period. Knowledge of hemodynamic data, presence of SVA and clinical characteristics in the acute infarction period were of no value in predicting the occurrence of SVA after hospital discharge patients having had an acute diaphragmatic infarction were found to have a higher incidence of SVA after hospital discharge.

Acute Disease↗
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

Measurement of S-T segment elevation in acute myocardial infarction in man. Comparison of a precordial mapping technique and the Frank vector system.

Precordial S-T segment mapping has been used to evaluate the extent of ischemic injury in patients with acute myocardial infarction. Because precordial S-T segment mapping is time-consuming and is limited to patients with anterior wall myocardial infarction, we evaluated the possibility of using the magnitude (ST-VM) and direction (ST-VD) of the S-T vector, derived from X, Y and Z leads of the Frank vector system, as a substitute for the precordial S-T segment mapping technique. Precordial S-T segment mapping and Frank system vectorcardiograms were simultaneously obtained in three groups: (1) nine normal subjects; (2) nine patients with persistent S-T segment elevation 2 to 15 months after acute anterior myocardial infarction; and (3) nine patients with acute anterior myocardial infarction studied on 41 occasions. For both systems the S-T segments were analyzed 20 and 60 msec after completion of inscription of the QRS complex. The sum of the S-T segment elevations for the 35 sites (sigma ST) and the number of sites (NST) in which S-T segment elevations exceeded 0.1 mv were computed for the precordial S-T maps. The ST-VM and ST-VD were calculated by standard formulas from X, Y and Z lead tracings of the Frank vector system. Good correlations were observed between: ST-VM and sigma ST (r = +0.818 and +0.791 at 20 and 60 msec, respectively, P less than 0.001); and ST-VM and NST (r = +0.773 and +0.705 at 20 and 60 msec, respectively, P less than 0.001). Furthermore, changes in the location of S-T segment elevations in serial precordial S-T segment maps were reflected by changes in ST-VD. Observations in patients with inferior wall myocardial infarction suggest that ST-VM and ST-VD can be serially followed in such patients. Thus, estimation of the magnitude and direction of the S-T vector is a simple alternative to standard precordial S-T segment mapping that allows for continuous monitoring of S-T segment elevations in all patients with acute myocardial infarction.

Acute Disease↗
PubMed1975

Echocardiographic observations on ventricular septal rupture complicating acute myocardial infarction.

Echocardiograms were performed on three patients with ventricular septal rupture complicating myocardial infarction. The pulmonary artery mean pressure was 30 mm Hg or more in all three patients. The size of the ventricular septal defect, determined at operation or autopsy, was 2 cm or greater in each patient. The salient echocardiographic abnormality was dilatation of the right ventricle. The direction of septal motion was normal in all the patients. The left atrial diameter was slightly increased in one patient and was normal in the other two. In one patient, and unusual pattern of mitral valve motion was seen. Complete closure of the reopening of the valve. This pattern was suggestive of increased blood flow through the mitral valve. Although some of these findings are nosspecific, the combination of echocardiographic findings may provide useful clues to the diagnosis of septal perforation.

Acute Disease↗
PubMed1975

High level positive end expiratory pressure (PEEP) in acute respiratory insufficiency.

Twenty-eight patients developed severe, progressive acute respiratory insufficiency despite aggressive application of conventional respiratory therapy. Application of increased PEEP (18 torr or greater) resulted in a significant decrease in QA/QT. Selection of the optimal levle of PEEP for each patient required serial determinations of QA/QT and measurement of cardiovascular response. The overall survival rate was 61 percent. Acute respiratory insufficiency was a proximate cause of death in only one patient. Four of the patients (14 percent) developed a pneumothorax following institution of high PEEP therapy. Cardiac output was not affected adversely at any level of PEEP up to 32 torr (44 cm H2O). We conclude that high levels of PEEP can be therapeutic for patients with refractory respiratory failure when combined with intermittent mandatory ventilation and careful cardiovascular monitoring. As with any therapy, the optimum dose should be tailored to each patient according to his needs and response.

Acute Disease↗