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Biomedical subjects

W Y Lew

Publications and source records attributed to W Y Lew.

48 records · Page 3Linked to original sources
PubMed1987

Influence of the pericardium on right and left ventricular filling in the dog.

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Risk of developing complete heart block during bedside pulmonary artery catheterization in patients with left bundle-branch block.

We examined the incidence of complete heart block (CHB) as a complication of pulmonary artery catheterization with balloon-tipped, flow-directed catheters in patients with left bundle-branch block (LBBB). The study group included 47 consecutive critically ill patients with LBBB in the medical intensive care and coronary care units, who underwent a total of 82 pulmonary artery catheterizations. Twenty-six patients had an acute myocardial infarction, 34 patients had severe congestive heart failure (Killip class III or class IV), and 15 patients died during their hospitalization. Thirty patients had an old LBBB (more than one month in age), nine patients had a new LBBB, and the age of the LBBB was indeterminate in eight patients. There were five episodes of CHB in the group of patients with old LBBB. However, none of these episodes were related to the pulmonary artery catheterization, since CHB occurred either prior to catheterization (one case) or from one to 16 days after the pulmonary artery catheter had been removed (four cases). There were no episodes of CHB related to the pulmonary artery catheterization procedure in the patients with either old LBBB or indeterminate-aged LBBB. There were two episodes of CHB in patients with new LBBB. In both patients, the CHB occurred one day after the pulmonary artery catheter had been inserted. In both patients, CHB developed after episodes of ventricular tachycardia that eventually resulted in their deaths. Although it is unlikely, we could not rule out the possibility that the CHB was related to the presence of the pulmonary artery catheter. We conclude that the incidence of CHB complicating pulmonary artery catheterization with balloon-tipped, flow-directed catheters in critically ill patients with old or indeterminate-aged LBBB is extremely low. Therefore, we do not recommend the routine placement of a temporary transvenous pacemaker in all patients with LBBB prior to pulmonary artery catheterization.

Aged↗
PubMed1986

Cardiopulmonary effects of cuprophane-activated plasma in the swine.

Hemodialysis with cuprophane membrane is associated with complement activation and the formation of anaphylatoxins. Frequently, it is also complicated by various adverse reactions which include hypoxemia and hemodynamic changes. This study examined the cardiopulmonary effects of cuprophane membrane on experimental animals. To support the hypothesis that these effects were mediated by complement activation products, the effects of zymosan-activated plasma and C5adesArg challenge on the same variables were compared. We showed that intravenous infusion of autologous cuprophane-activated plasma into swine produced severe pulmonary hypertension, hypoxemia and leukopenia. In addition, mean systemic arterial pressure fluctuated and cardiac output fell. Infusion of zymosan-activated plasma produced similar results, suggesting that complement activation products are responsible for these alterations. Similar responses to porcine C5adesArg infusion suggested further that this polypeptide was the mediator. When swine were subjected to extracorporeal circulation using cuprophane membrane but without dialysis, acute pulmonary hypertension was seen preceding the onset of significant leukopenia. These data suggest that blood contact with cuprophane membrane produces both pulmonary and systemic hemodynamic changes, which are mediated by complement activation products. Furthermore, these products and/or other humoral factors, but not leukoagglutination, cause the pulmonary hypertension.

Animals↗
PubMed1986

Hysteresis of left ventricular end ejection pressure-dimension relations after acute pressure loading in the intact canine heart.

The left ventricular end systolic pressure-volume relation of the isolated canine heart is linear and independent of the loading conditions. The effects of acute pressure loading on the left ventricular end ejection pressure-length relations were studied in the intact canine heart. The lengths of two wall segments of the left ventricle parallel to the minor axis were measured with pairs of miniature piezoelectric crystals. At two levels of filling pressure, with and without control of heart rate, acute increases in left ventricular afterload were produced for six successive beats by occluding the thoracic aorta. After abrupt release of this occlusion, at left ventricular end diastolic pressure less than 10 mmHg, end ejection lengths were longer than before the occlusion for both segments despite the same or lower end ejection pressures. When heart rate was not controlled the mean(SD) difference in end ejection length was 0.46(0.21) mm (n = 100). When heart rate was controlled by atrial pacing after autonomic blockade the difference was 0.37(0.11) mm (n = 80). In contrast, at left ventricular end diastolic pressure greater than 10 mmHg there was no significant difference between end ejection lengths before and after release of the aortic occlusion. Gradual release of the aortic occlusion over 4-5 beats produced clockwise hysteresis of the left ventricular end ejection pressure-length relation when left ventricular end diastolic pressure was less than 10 mmHg. No hysteresis occurred when left ventricular end diastolic pressure was greater than 10 mmHg. Hysteresis of the end systolic pressure-dimension relation was also seen when major and minor axis dimensions of the left ventricular were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Substance P, 5-hydroxytryptamine, and bradykinin stimulate abdominal visceral afferents.

To determine if chemicals produced endogenously within the gastrointestinal system stimulate abdominal visceral sensory endings, we recorded the response of 42 A- and 25 C-fibers in the splanchnic nerve of cats as substance P (10-20 micrograms), 5-hydroxytryptamine (5-HT, 100-200 micrograms), or bradykinin (10 micrograms) was injected into the descending thoracic aorta. Approximately half of the sensory endings responded to each chemical. However, significantly more C- than A-fiber endings responded to 5-HT (64 vs. 39%) and bradykinin (76 vs. 41%). Most C-fiber endings were insensitive to external mechanical stimuli, supporting the concept that these endings are primarily chemosensitive. In contrast, most A-fiber endings were quite sensitive to external mechanical stimuli. Additionally, more A-fiber endings located in contractile (gut or vasculature) than in noncontractile (pancreas, liver, or spleen) regions responded to 5-HT (58 vs. 19%), bradykinin (67 vs. 15%), and substance P (57 vs. 29%), a response that frequently occurred coincident with the development of chemically induced gut contractions. Thus many A-fiber endings are primarily sensitive to mechanical stimuli. However, 15-30% of the A-fiber endings located in noncontractile regions responded to chemicals, although the endings likely were removed from the mechanical effects of these chemicals. Since these A-fiber endings are also quite sensitive to external mechanical stimuli, they may be polymodal in their function. We conclude that abdominal visceral sensory endings are not homogeneous in function and are stimulated by several chemicals produced endogenously within the gastrointestinal system, including substance P, 5-HT, and bradykinin.

Abdomen↗
PubMed1986

Regional comparison of midwall segment and area shortening in the canine left ventricle.

We used ultrasonic segment length gauges to examine the regional behavior of midwall fibers at different sites around the left ventricular minor axis in 12 anesthetized dogs. In six dogs (group I) with circumferentially oriented midwall gauges, significantly greater shortening of anterior than lateral or posterior wall segments was demonstrated over a range of left ventricular end-diastolic pressures from 2 to 18 mm Hg. Normalized end-diastolic segment lengths increased more in the anterior wall as end-diastolic pressure increased, suggesting that regional differences in diastolic distensibility may in part account for the observed shortening differences. To examine the extent to which shortening of longitudinally oriented fibers of the subendocardium and subepicardium might influence the behavior of the midwall circumferential fibers, we implanted mutually perpendicular midwall gauges circumferentially and longitudinally in the anterior and posterior walls in six dogs (group II). Longitudinal shortening of midwall fibers was negligible at low end-diastolic pressures, but increased significantly at higher end-diastolic pressures. In the anterior wall, there was greater circumferential than longitudinal shortening, whereas, in the posterior wall, shortening was similar in the two directions. Finally, we calculated the midwall area subtended by the mutually perpendicular gauges and found the systolic change in midwall area to be similar for the anterior and posterior walls at all end-diastolic pressures. We conclude that midwall fibers demonstrate considerable nonuniformity of contraction at different sites around the minor axis. This finding may be related in part to regional differences in diastolic distensibility or in functional interactions between fiber layers. Despite these complex regional, directional, and volume dependent differences in midwall segment function, the systolic changes in midwall area did not vary regionally. Thus, different midwall sites around the minor axis circumference appear to have similar overall contributions to the ejection of blood.

Animals↗
PubMed1985

Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle.

We examined the influence of left ventricular end-diastolic pressure (LVEDP) on the mechanical interaction between ischemic and nonischemic areas during acute myocardial ischemia. Circumferentially oriented ultrasonic segment gauges were implanted in the midwall of the anterior apex and posterior apex of the left ventricle in seven anesthetized dogs. Stroke volume was measured with a flow probe around the ascending aorta in five of these animals. We varied LVEDP with vena caval occlusion and dextran infusions to three matched levels (7, 12, and 19 mm Hg) before and 30 min after complete occlusion of the mid left anterior descending coronary artery. With acute ischemia, the anterior apex or ischemic zone demonstrated marked segmental lengthening during isovolumetric systole (end-diastole to aortic valve opening) and akinesis during the ejection phase (aortic valve opening to closure). In the posterior apex or nonischemic area, isovolumetric shortening increased and ejection phase shortening decreased during acute ischemia when compared with those under control conditions at the same LVEDP. Thus, a portion of the shortening generated by the nonischemic area was expended in stretching the ischemic zone during isovolumetric systole, thereby reducing the amount of ejection phase shortening. As LVEDP was increased, there was a parallel decrease in both the amount of isovolumetric lengthening in the ischemic zone and the isovolumetric shortening in the nonischemic area. As a result, acute ischemia produced less of a reduction in ejection phase shortening in the nonischemic area and in stroke volume at high as compared with low LVEDP. We conclude that the ischemic zone imposes a mechanical disadvantage on the nonischemic area, the magnitude of which is directly proportional to the amount of isovolumetric lengthening or bulge in the ischemic zone. An increase in LVEDP during acute ischemia improves regional and global ventricular function by both the Frank-Starling mechanism in the nonischemic (but not the ischemic) area and by reducing the mechanical disadvantage that the ischemic zone imposes on the nonischemic area.

Animals↗
PubMed1985

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, end-diastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant "compensatory" increase in ejection shortening in nonischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1983

Regional circumferential lengthening patterns in canine left ventricle.

We employed sonomicrometers in open-chest dogs to study lengthening of short segments of circumferentially oriented myocardium located at the base, midportion, and apex of the anterior left ventricular free wall. Left ventricular pressure was varied by inferior vena caval occlusion and volume expansion. Diastole was divided into rapid and slow lengthening phases. Rapid lengthening was completed first at the basal site at each of three successive levels of left ventricular diastolic pressure (LVDP). At the base, significant further lengthening occurred during the slow lengthening phase while at the apex virtually all lengthening was completed during the rapid phase. At low LVDPs, peak lengthening rates (dl/dt) were greatest at the apex. As LVDP was increased, regional differences in dl/dt diminished. These results indicate that there is regional variation in the timing of the phases of diastole and in lengthening patterns of the left ventricle. The volume-dependent variation in lengthening rates that we observed is consistent with the concept of regional differences in elastic recoil, which may contribute to active ventricular filling.

Animals↗
PubMedDate not supplied

Torsades de pointes and sudden death in a patient with a permanent pacemaker.

This report describes a patient with a functioning permanent pacemaker who developed torsades de pointes. Although overdrive cardiac pacing has been used to suppress this arrhythmia, cardiac pacing was not protective in this patient. This case also illustrates the difficulty in interpreting Q-T intervals in the presence of paced beats.

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