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Biomedical subjects

M B Fowler

Publications and source records attributed to M B Fowler.

65 records · Page 4Linked to original sources
PubMed1982

Comparison of haemodynamic responses to dobutamine and salbutamol in cardiogenic shock after acute myocardial infarction.

Nine patients with critically reduced cardiac output after acute myocardial infarction underwent a single cross-over comparison of dobutamine and salbutamol to compare the haemodynamic effects of these drugs, which have, respectively, predominantly beta 1-adrenergic and beta 2-adrenergic agonist activity. The responses were used to select the more appropriate treatment for individual patients. Only relatively small responses were obtained: those with poorest baseline measurements tended to show the least effect. When the results from the series were averaged, dobutamine (250-750 microgram/min) caused a small but progressive increase in cardiac index (1.8 to 2.2 1/min/m2) throughout the dose range. Systemic blood pressure was not increased, and calculated systemic vascular resistance fell from 25 to 19 units. Heart rate rose from 107 to 118 beats/min and stroke index from 17 to 19 ml/beat/m2. Pulmonary artery end-diastolic pressure fell from 18 to 15 mm Hg. Salbutamol (10-40 microgram/min) produced a similar progressive increase in cardiac index, from 1.6 to 2.21/min/m2. Systemic blood pressure was not altered, and systemic vascular resistance fell from 25 to 20 units. Heart rate rose from 105 to 119 beats/min and stroke index from 16 to 19 ml/beat/m2. Pulmonary artery end-diastolic pressure did not fall. Dobutamine and salbutamol have closely similar haemodynamic effects when used in cardiogenic shock after acute myocardial infarction. Both drugs increase cardiac index but heart rate also rises, and the increase in stroke index is relatively small. Mean arterial pressure is altered little by either agent, but dobutamine (in contrast with dopamine) tends to reduce pulmonary artery end-diastolic pressure, which may be beneficial.

Aged↗
PubMed1982

Role of labetalol in acute myocardial infarction.

1 The role of labetalol in managing acute myocardial infarction is reviewed. 2 After intravenous infusion labetalol lowers blood pressure in patients with increased blood pressure associated with acute myocardial infarction. 3 Although average heart rate was decreased, cardiac index fell only slightly and stroke index was substantially unchanged. 4 In patients whose pretreatment pulmonary artery end-diastolic pressures were increased, labetalol induced decreases, whereas in the presence of normal pressures, these were unchanged. 5 It is concluded that labetalol infusion in patients with acute myocardial infarction is unlikely to precipitate heart failure and is likely to be of value in reducing myocardial oxygen requirement.

Acute Disease↗
PubMed1981

Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction.

Twelve patients with acute myocardial infarction and radiological evidence of pulmonary oedema were observed in whom the left atrial pressure, measured indirectly as pulmonary artery end-diastolic pressure, was not critically increased (range 5-12 mm Hg with reference to sternal angle). Eight of the patients had been treated with frusemide, but only six had responded: hence in at least half of the series diuresis could not account for the anomalous finding. Six patients with low cardiac output were given infusions to expand plasma volume. Appreciable increments in mean values for cardiac index (1.6 to 2.0 1/min/m2), stroke index (18 to 23 ml/beat/m2), mean arterial pressure (65 to 86 mm Hg), and pulmonary artery end-diastolic pressure (8 to 15 mm Hg) were recorded. This group, and the remaining six patients with higher cardiac output, survived to leave hospital. Delay in radiographic clearing after a fall of left atrial pressure was a possible explanation for the relatively low pulmonary artery end-diastolic pressures, especially in the patients treated successfully with diuretics. Other mechanisms, such as alterations in pulmonary vascular permeability, might also have contributed to the syndrome. Pulmonary oedema without a critical increase in the left atrial pressure is unusual in acute myocardial infarction but the therapeutic implications are important. Withdrawal;of diuretics may be indicated, and in some cases expansion of plasma volume may lead to striking clinical improvement.

Aged↗
PubMed1981

Comparison of haemodynamic responses to dopamine and salbutamol in severe cardiogenic shock complicating acute myocardial infarction.

Twelve patients with severe persistent cardiogenic shock complicating acute myocardial infarction underwent single crossover treatment with intravenous dopamine and salbutamol to determine the more beneficial therapy. Salbutamol (10 to 40 microgram/min) reduced systemic vascular resistance and progressively increased both cardiac index and stroke index. Heart rate increased from 95 to 104 beats/min. Changes in mean arterial pressure and pulmonary artery end-diastolic pressure were small and insignificant. Dopamine infusion at rates of 200 and 400 micrograms/min also increased cardiac index and stroke index. Systemic vascular resistance fell slightly but mean arterial pressure rose from 57 to 65 mm Hg. Heart rate increased from 95 to 105 beats/min. Changes in pulmonary artery end-diastolic pressure were again small and insignificant. Dopamine infusion at 800 micrograms/min caused an appreciable increase in systemic vascular resistance; a further increment in mean arterial pressure was observed, though cardiac index fell slightly. Heart rate and pulmonary artery end-diastolic pressure rose steeply. Salbutamol, a vasodilator, increased cardiac output in patients with cardiogenic shock complicating acute myocardial infarction but did not influence blood pressure. If correction of hypotension is essential dopamine in low doses may be the preferred agent. Doses of 800 microgram/min, which is within the therapeutic range, worsen other manifestations of left ventricular dysfunction.

Albuterol↗
PubMed1980

Synergistic effects of a combined salbutamol-nitroprusside regimen in acute myocardial infarction and severe left ventricular failure.

The haemodynamic effects of a simultaneous infusion of salbutamol and nitroprusside were measured in 20 patients with acute myocardial infarction and severe left ventricular failure. Six patients also had clinical manifestations of cardiogenic shock. Ten patients received salbutamol first with the subsequent addition of nitroprusside; in the other 10 patients nitroprusside was infused first. Salbutamol was infused at a constant rate of 20 micrograms/min in all patients, while the dose of nitroprusside, which averaged 51.25 micrograms/min, was adjusted to reduce left ventricular filling pressure (measured as pulmonary artery end-diastolic pressure) to approximately 15 mm Hg with reference to sternal angle. Cardiac index increased in all patients from a mean of 1.8 to 2.6 l/min/m2 while pulmonary artery end-diastolic pressure fell significantly from 24 to 16 mm Hg. The adverse effects were small in most patients: heart rate did not increase significantly and systolic arterial pressure fell on average from 112 to 96 mm Hg. Ten of the 20 patients survived to leave hospital. Nitroprusside accounted for most of the fall in filling pressure irrespective of treatment sequence, whereas both drugs contributed to the augmented cardiac output. The haemodynamic benefits of this combined regimen were considerably greater than those achieved by either drug alone. Thus salbutamol and nitroprusside have synergistic effects which influence favourably the two principal manifestations of left ventricular dysfunction after extensive myocardial infarction.

Aged↗
PubMedDate not supplied

Assessment of left ventricular wall motion abnormalities with the use of color kinesis: a valuable visual and training aid.

Accurate interpretation of left ventricular segmental wall motion by echocardiography is an important yet difficult skill to learn. Color-coded left ventricular wall motion (color kinesis) is a tool that potentially could aid in the interpretation and provide semiquantification. We studied the usefulness of color kinesis in 42 patients with a history of congestive cardiomyopathy who underwent two-dimensional echocardiograms and a color kinesis study. The expert's reading of the two-dimensional wall motion served as a reference for comparison of color kinesis studies interpreted by the expert and a cardiovascular trainee. Correlation between two-dimensional echocardiography and the expert's and trainee's color coded wall motion scores were r = 0.83 and r = 0.67, respectively. Reproducibility between reviewers and between operators was also assessed. Interobserver variability for color-coded wall motion showed a correlation of r = 0.78. Correlation between operators was also good; r = 0.84. Color kinesis is reliable and appears promising as an adjunct in the assessment of wall motion abnormalities by echocardiography. It is both a valuable visual aid, as well as a training aid for the cardiovascular trainee.

Adult↗
PubMedDate not supplied

Joplin's neuroma or compression neuropathy of the plantar proper digital nerve to the hallux: clinicopathologic study of three cases.

Both nonsurgical and surgical treatment of compressive and/or entrapment neuropathy of the plantar proper digital nerve to the hallux, also known as Joplin's neuroma, are very uncommon in the literature. The condition of perineural fibrosis of this nerve was first described in 1971 by Joplin. Diagnosis of this nerve in a localized pathologic process based on physical exam and surgical pathology and noniatrogenic etiology are discussed. Three case studies of Joplin's neuroma are followed through the treatment course from initial presentation to postoperative follow-up.

Adult↗
PubMedDate not supplied

Cardiac sarcoidosis: response to steroids and transplantation.

From 1976 to 1986, six cases of cardiac sarcoidosis have been documented by myocardial biopsy in three of five instances; on examination of the explanted heart after transplantation in two, and at autopsy in one patient. Right ventricular end-diastolic pressure was elevated in all four patients with right ventricular involvement with sarcoidosis. Of three patients treated with steroids, improvement in ventricular function and decrease in arrhythmia occurred in two, whereas failure to respond led to transplantation in the other patient. Two further patients have undergone heart transplantation, one for resistant ventricular arrhythmia and the other for congestive heart failure. No recurrence of sarcoidosis has occurred in the grafts. Because two of five patients had sarcoidosis diagnosed on gross examination, a negative endomyocardial biopsy does not exclude the diagnosis of myocardial sarcoidosis, which should therefore be pursued in the setting of unexplained heart failure, conduction abnormalities, and ventricular arrhythmia, particularly when right ventricular end-diastolic pressure is raised. Steroids may result in improvement in some patients even in the presence of severe morphological damage. Heart transplantation may be performed without increased risk of recurrence of sarcoidosis.

Adult↗