Biomedical subjects

S Magder

Publications and source records attributed to S Magder.

81 records · Page 5Linked to original sources

PubMed1985

Effects of pleural pressure and abdominal pressure on diaphragmatic blood flow.

The aim of this experiment was to determine if blood flow to the diaphragm is affected by generating the transdiaphragmatic pressure mainly with positive abdominal pressure or mainly with negative pleural pressure, during both sustained and intermittent diaphragmatic contractions. Diaphragmatic blood flow was measured in anesthetized mongrel dogs by the radionuclide-labeled microsphere method. Sustained and intermittent tetanic diaphragmatic contractions were produced with 1) free abdomen and closed chest (high negative pleural pressure) and 2) bound abdomen and open chest (high positive abdominal pressure). During sustained contractions, diaphragmatic blood flow at maximum levels of activation was significantly higher with negative pleural pressure (P less than 0.05). In contrast with this, intermittent diaphragmatic contractions did not yield a significant difference between diaphragmatic blood flow with negative pleural pressure and with positive abdominal pressure at maximal levels of transdiaphragmatic pressure. During both sustained and intermittent contractions, blood pressure, as measured from the carotid artery, did not vary significantly between negative pleural pressure and positive abdominal pressure. We conclude that during sustained tetanic diaphragmatic contractions, diaphragmatic blood flow is obstructed by high positive abdominal pressures, but during intermittent diaphragmatic contractions, high positive abdominal pressures do not affect total blood flow, since any inhibition of blood flow during the contractile period can be compensated for during the relaxation period between contractions.

Abdomen↗

PubMed1985

Respiratory muscle and organ blood flow with inspiratory elastic loading and shock.

Since respiratory muscles fail when blood flow is inadequate, we asked whether their blood flow would be maintained in severe hypotensive states at the expense of other vital organs (brain, heart, kidney, gut, spleen). We measured blood flow (radiolabeled microspheres) to respiratory muscles and vital organs in 11 dogs breathing against an inspiratory elastic load, first with normal blood pressure (BP) and then hypotension produced by cardiac tamponade. With the elastic load alone, there was no change in BP or cardiac output; diaphragmatic blood flow (Qdi) increased from 12.8 +/- 7.0 to 34.1 +/- 15.6 ml/100 g, and total respiratory muscle flow (QTR) increased from 56.5 +/- 19.1 to 97.4 +/- 36.5 ml/100 g, but except for the brain, there was no change in blood flow to other organs. With tamponade (mean BP = 79 +/- 16 mmHg), flow decreased to all organs, whereas Qdi (39.0 +/- 19.4) did not change. QTR decreased, but not significantly, to 88.6 +/- 49.5. With more tamponade (mean BP = 53 +/- 13 mmHg), flow to all vital organs decreased as well as QTR (57.9 +/- 47.18), but Qdi did not significantly decrease and had the same relationship to respiratory force as with normal BP. Thus, with severe inspiratory elastic loading and severe hypotension, the diaphragm and external intercostal muscles did most of the respiratory work, and their flow was maintained at the expense of other vital organs.

Animals↗

PubMed1985

Collateral sources of costal and crural diaphragmatic blood flow.

We measured the contribution of aortic, internal mammary, and intercostal arteries to the blood flow to the costal and crural segments of the diaphragm and other respiratory muscles in seven dogs breathing against a fixed inspiratory elastic load. We used radiolabeled microspheres to measure the blood flow with control circulation, occlusion of the aorta distal to the left subclavian artery, combined occlusion of the aorta and both internal mammary arteries, and occlusion of internal mammary arteries alone. With occlusion of the aorta distal to the left subclavian artery, blood flow to the crural diaphragm decreased from 40.3 to 23.5 ml . min-1 X 100 g-1, whereas costal flow did not change significantly (from 41.7 to 38.1 ml . min-1 . 100 g-1). Blood flows to the sternomastoid and scalene muscles (above the occlusion) increased by 200 and 340%, respectively, whereas flows to the other respiratory muscles did not change significantly. Blood flows to organs above the occlusion either remained unchanged or increased, whereas flows to those below the occlusion all decreased. When the internal mammary artery was also occluded, flows to the crural segment decreased further to 12.1 and costal flow decreased to 20.4 ml X min-1 X 100 g-1. Internal mammary arterial occlusion alone in two dogs had no effect on diaphragmatic flow. In conclusion, intercostal collateral vessels are capable of supplying a significant proportion of blood flow to both segments of the diaphragm but the costal segment is better served than the crural segment.

Airway Resistance↗

PubMed1985

Assessment of myocardial stress from early ambulatory activities following myocardial infarction.

Little is known of the magnitude of the stress imposed on the heart by ambulatory activities following infarction. Heart rate, blood pressure, and rhythm provide simple and important estimates of these potential stresses. We therefore measured these variables in 32 patients during sitting, standing, and walking in the first two days following myocardial infarction. Ambulatory activities caused only a small increase in heart rate, with a maximum increase of 9 beats/minute during walking. The blood pressure was either unchanged or decreased during activity. In six other patients, we also measured central hemodynamics during the same activities. The wedge pressure fell with sitting and standing and remained low after walking. All activities were well tolerated. The major problem was hypotension; this was associated with chest pain in one patient, dizziness in four and shortness of breath in two. Most of the patients with hypotension were taking nitrates. In conclusion, mild ambulatory activities produce little stress for the myocardium and can be permitted in the first few days following infarction as long as blood pressure is measured.

Adult↗

PubMed1983

Validity of the hepatojugular reflux as a clinical test for congestive heart failure.

This study describes observations designed to test the validity of the hepatojugular reflux as an indicator of actual or incipient heart failure. The central venous pressure (CVP) could be predicted from the height of the jugular venous pulsations in 44 of 48 comparisons. In the remaining comparisons, discrepancies ranged from 5 to 7 mm Hg. In patients with normal resting cardiac function, abdominal compression did not cause an increase in CVP of greater than 2 mm Hg (2.7 mm H2O). In 16 of 19 patients with impaired function, CVP increased by greater than or equal to 3 mm Hg. The increase in CVP was estimated from neck veins to within 2 mm Hg in all but 3 instances. CVP stabilized by 10 seconds and did not change over the subsequent 60 seconds. Abdominal compression caused no consistent change in cardiac output. Changes in venous pressure could not be attributed to changes in esophageal pressure or to compression of the heart by elevation of the diaphragm. Observations were consistent with the hypothesis that an increase in right-sided cardiac filling pressures resulting from abdominal compression carried out as described here, reflects both the volume of blood in the abdominal veins and the ability of the ventricles to respond to increased venous return, and constitutes a useful clinical test for detecting congestive cardiac failure. An increase of 3 cm in the height of neck vein distention is a reasonable upper limit of normal.

Abdomen↗

PubMed1983

Thoracicoabdominal mechanics during resuscitation maneuvers.

The importance of intrathoracic pressure in generating blood flow during cardiopulmonary resuscitation has recently been emphasized. The purpose of this study was to investigate the factors involved in generating intrathoracic pressure. Studies were performed in anesthetized paralyzed dogs with the circulation intact. Balloon-tipped catheters were placed in the abdomen and esophagus for measurement of intra-abdominal and intrathoracic pressures and cannula placed in the airway for airway pressure. The following four maneuvers were studied: (1) chest compression with open airway; (2) chest compression with closed airway; (3) pulmonary inflation to transpulmonary pressure (TP) of 30 cm H2O (TP = 30); and (4) chest compression plus pulmonary inflation (TP = 30). We found that under static conditions, chest compression alone produced small positive intrathoracic pressures (9 +/- 8 cm H2O), but these could be increased by closing the airway pressure (18 +/- 6 cm H2O) or inflating the lungs (15 +/- 7 cm H2O). The combination of inflating the lung and compressing the chest produced the highest intrathoracic pressure (48 +/- 18 cm H2O; p less than 0.001). The pressure developed was highly variable and the distribution of pressures within the thorax was not uniform. As the intrathoracic pressure became large, a pressure gradient developed from thorax to abdomen, and the diaphragm everted; this pressure gradient could divert blood from the brain.

Abdomen↗

PubMed1982

Comparison of cardiovascular response to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone in patients with chronic ischemic heart disease.

The cardiovascular responses to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone were evaluated by upright bicycle ergometry during equilibrium-gated blood pool scintigraphy in 24 men, mean age 59 +/- 8 years, with chronic ischemic heart disease. Combined static-dynamic effort and the postprandial state elicited a peak cardiovascular response similar to that of dynamic effort alone; work load 643 +/- 156 and 638 +/- 161 vs 650 +/- 153 kg-m/min, respectively; heart rate 147 +/- 14 and 145 +/- 14 vs 143 +/- 17 beats/min; systolic pressure 195 +/- 26 and 200 +/- 25 vs 197 +/- 25 mm Hg; and rate-pressure product 286 +/- 48 and 292 +/- 55 vs 282 +/- 52. Heart rate, intraarterial systolic and diastolic pressures, rate-pressure product and ejection fraction were similar for the three test conditions at the onset of ischemia and at peak effort. The prevalence and extent of exercise-induced ischemic left ventricular dysfunction, ST-segment depression, angina pectoris and ventricular ectopic activity were also similar during the three test conditions. Direct and indirect measurements of systolic and diastolic blood pressure were highly correlated. The onset of ischemic ST-segment depression and angina pectoris correlated as strongly with heart rate alone as with the rate-pressure product during all three test conditions. The cardiovascular response to combined static-dynamic effort and to postprandial dynamic effort becomes more similar to that of dynamic effort alone as dynamic effort reaches a symptom limit. If significant ischemic and arrhythmic abnormalities are absent during symptom-limited dynamic exercise testing, they are unlikely to appear during combined static-dynamic or postprandial dynamic effort. This simplifies, the task of formulating guidelines for physical effort in patients with chronic ischemic heart disease, especially in providing "clearance" to perform avocational and vocational tasks involving combined static-dynamic and postprandial dynamic effort.

Aged↗

PubMed1981

The effect of swimming on patients with ischemic heart disease.

Swimming is frequently recommended for cardiac rehabilitation, but little is known of its physiologic consequences in ischemic heart disease. Eight males who had had a myocardial infarction 8-17 months before the study were exercised to exhaustion or angina with 10 W/min-1 ramp on a cycle ergometer in sitting and supine positions. Oxygen uptake (VO2) was continuously measured to monitor the physiologic power requirement. All eight patients were taking beta blockers and four were taking digoxin. During sitting cycling, angina occurred in four and ST depression in five; during supine cycling, angina occurred in five and ST depression in six. VO2 was then measured while they swam at their own comfortable speed (mean 0.43 m/sec-1) in a swimming flume at water temperatures of 25.5 degrees C and 18 degrees C. In six, the water speed was gradually increased until they were limited by symptoms. Comfortable swimming at 25.5 degrees C was 87% (1.28 1/min-1) and at 18 degrees C 89% (1.30 1/min-1) of sitting peak VO2, while heart rates were 92% and 91% respectively. The mean peak VO2 and heart rate did not differ significantly between bicycle and swim tests (peak VO2 sitting 1.49 +/- 0.23, supine 1.42 +/- 0.24, 25.5 degrees C 1.60 +/- 0.17, 18 degrees C 1.52 +/- 0.19 1/min-1). Only two patients reported angina while swimming in warm water and one in cold water, although ST depression occurred in six in both swims. The subjective comfort and large muscle groups involved make swimming a good exercise, but the high relative energy cost and failure to identify ischemic symptoms indicate caution in cardiac patients, especially if their swimming skills are poor.

Aged↗

PubMedDate not supplied

Effects of equipotent blocking doses of acebutolol, acebutolol's primary metabolite, and propranolol on left ventricular hemodynamics in conscious awake dogs.

In six conscious dogs we compared the hemodynamic effects of propranolol, acebutolol, and acebutolol's primary metabolite at equipotent beta-blocking doses. Aortic pressure, heart rate, left ventricular end-diastolic pressure, dP/dt, and aortic flow velocity were measured 3 weeks after sterile surgery during three infusions of each drug. Only one drug was given on each day. The equipotent beta-blocking dose of each drug was obtained by comparing isoproterenol dose-response curves. All three drugs produced a fall in dP/dt. Left ventricular end-diastolic pressure increased in most dogs, but this was only significant for acebutolol. The heart rate tended to fall and the blood pressure rise, but this was variable and not significant. The concentration of the equipotent blocking dose of acebutolol was 44 times that of propranolol, and while the concentration of acebutolol's metabolite was 1.6 times that of acebutolol. In conclusion, at a concentration similar to acebutolol, acebutolol's metabolite has heart rate blocking and myocardial depressive effects similar to those of propranolol and acebutolol.

Acebutolol↗