Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inotropic effects of albumin were studied in 94 seriously injured patients who received an average of 14.5 transfusions, 9.2 liters of crystalloid and 0.9 liters of plasma prior to end of operation; 46 patients, by random selection, received added albumin averaging 31 gm during operation, 198 gm during the early postoperative period of extravascular fluid sequestration, and 395 gm during the first 4 days of the later fluid mobilization period. Left ventricular stroke work index (LVSWI) was plotted against pulmonary wedge pressure (Ppw) in 22 patients who had indwelling thermistor pulmonary artery catheters at the time of the first study. Calculated heart work units (WU) were derived from the pulse pressure, mean arterial pressure, pulse rate, and central venous pressure (CVP) in patients without LVSWI measurements. Albumin supplementation increased serum albumin (4.2 vs. 2.9 gm%), plasma volume, CVP (15 vs. 9 cm H2O), but did not alter red cell volume (1,531 vs. 1,519 ml). The ratio of LVSWI/Ppw fell in albumin patients (1.9 +/- 1.6 vs. 4.8 +/- 1.8), and the ratio of WU/CVP was significantly depressed in albumin patients (4.9 +/- 2.3 vs. 7.3 +/- 2.1). The slopes of the LVSWI/Ppw and WU/CVP were shifted to the right in albumin patients. This negative inotropic effect was associated with impaired oxygenation, as reflected by an increased ratio of inspired oxygen per arterial oxygen tension (0.62 +/- 0.06 vs. 0.33 +/- 0.1). Finally, 24 of the 46 albumin-treated patients were digitalized for heart failure, compared to only 11 of the 48 nonalbumin patients. Pending subsequent studies, albumin should be considered a potentially negative inotropic agent.
 ...
PMID:Negative inotropic effect of albumin resuscitation for shock. 46 73

To compare the hemodynamic effects of prazosin and nitroprusside in patients with severe congestive heart failure, nine patients with heart failure refractory to conventional therapy received oral prazosin and intravenous nitroprusside administered so as to produce a similar decrease in left ventricular filling pressure in each patient. By this comparison, both drugs produced similar decreases in mean right atrial pressure, mean pulmonary arterial pressure and systemic and pulmonary vascular resistance. However, with nitroprusside, cardiac index increased more (+0.97 versus +0.73 liters/min per m2, P less than 0.01) and mean arterial pressure decreased less (-13.7 versus -18.3 mm Hg, P less than 0.05) than with prazosin. Both drugs produced similar changes in stroke volume index (+11.7 cc/beat per m2 with nitroprusside and +12.5 with prazosin) and stroke work index (+8.1 g-m/m2 with nitroprusside and +6.6 with prazosin). Therefore, the differences in the hemodynamic responses observed with the two agents were due to the significantly greater decrease in heart rate with prazosin (-8 beats/min) than with nitroprusside (-2 beats/min, P less than 0.05). These clinical data support experimental evidence suggesting that there is a significant negative chronotropic action of prazosin independent of its peripheral vascular effects.
 ...
PMID:Differences in hemodynamic effects of nitroprusside and prazosin in severe chronic congestive heart failure: evidence for a direct negative chronotropic effect of prazosin. 46 69

The persistence of the hemodynamic effects of prazosin was studied in 12 patients with chronic congestive heart failure. Multidose evaluation involving five 5-mg doses showed the initial decrease in systemic vascular resistance and increase in cardiac index, stroke work index, and stroke volume index to be transient. Doubling the dose did not restore effect. Modest decreases in pulmonary capillary-wedge and mean arterial pressures persisted throughout the study. In six patients, plasma prazosin concentration measured at times of hemodynamic observations showed the initial hemodynamic effect of prazosin to attenuate upon further administration despite mean plasma concentrations that exceeded those measured after the first dose. In patients with chronic heart failure, resting hemodynamic studies suggest a rapid attenuation of prazosin-mediated hemodynamic effect in the presence of adequate plasma concentration. Recognizing this phenomenon, if long-term prazosin therapy for congestive heart failure is contemplated, we suggest the hemodynamic response in individual patients be monitored.
 ...
PMID:Attenuation of prazosin effect on cardiac output in chronic heart failure. 47 64

Hemodynamic changes during exercise were evaluated in 20 patients with severe, chronic congestive heart failure. Two groups were identified by their stroke work response to maximal exercise. Group I (eight patients) showed an increase in stroke work index. This occurred because the stroke volume increased and the difference between mean systolic pressure and left ventricular filling pressure increased. Group II (12 patients) showed a decrease in stroke work index. This occurred because stroke volume decreased while the difference between mean systolic pressure and left ventricular filling pressure did not change. Despite hemodynamic differences, the groups could not be distinguished by the usual clinical criteria for heart failure including etiology, New York Heart Association functional class, heart size on chest X-ray film or duration of heart failure. Clinical criteria are relatively insensitive in predicting the exercise hemodynamics of any given patient with chronic severe heart failure. Determining the exercise hemodynamics may be helpful as a means of assessing left ventricular functional reserve in heart failure. Prognostic implications, drug therapy and prescription of activities may require adjustment based on this spectrum of hemodynamic response to exercise in patients with chronic heart failure.
 ...
PMID:Detection of left ventricular functional reserve by supine exercise hemodynamics in patients with severe, chronic heart failure. 49 99

Hemodynamic response to exercise before and 10 minutes after propranolol (5 mg intravenously) was studied in 10 young patients with pure mitral stenosis who had normal sinus rhythm and no cardiac failure. After propranolol the mean heart rate and cardiac index at rest were lower than during the control state (respectively, 95 +/- 4 versus 82 +/- 3 beats/min, P less than 0.005; 3.4 +/- 0.2 versus 2.8 +/- 0.1 liters/min per m2, P less than 0.025). As a result, the mean pulmonary wedge pressure and mean mitral valve gradient at rest were lower (respectively, 22 +/- 2 versus 18 +/- 2 mm Hg, P less than 0.005; 24 +/- 2 versus 17 +/- 2 mm Hg, P less than 0.001). During exercise after propranolol the values of pulmonary wedge pressure and mitral valve gradient were lower than control values during exercise (respectively, 39 +/- 3 versus 30 +/- 2 mm Hg, P less than 0.005; 44 +/- 3 versus 32 +/- 3 mm Hg, P less than 0.005), again because of the lower heart rate and cardiac index (130 +/- 6 versus 104 +/- 6 beats/min, P less than 0.001; 4.6 +/- 3 versus 3.7 +/- 2 liters/min per m2, P less than 0.01). Left ventricular end-diastolic pressure and stroke index showed no significant changes. Thus, propranolol may benefit patients with pure mitral stenosis with sinus rhythm and no cardiac failure whose symptoms occur during those reversible conditions characterized by an increase in heart rate or cardiac output, or both.
 ...
PMID:Hemodynamic response to exercise after propranolol in patients with mitral stenosis. 49 1

In order to determine and compare the pharmacodynamic responses to single and multiple dose prazosin therapy in cardiac failure, 14 patients with severe low-output heart failure underwent central and regional hemodynamic measurements after random placement in one of two prazosin dosing schedules. A single 5 mg oral dose of prazosin (Group A, no. = 7) significantly increased the cardiac index and stroke volume index while significantly decreasing systemic, pulmonary and pulmonary capillary wedge pressures and vascular resistances. Hepatic plasma flow and limb blood flow increased after the single dose. Striking attenuation of these hemodynamic effects occurred when the same dose was administered after 24 hours of pretreatment with oral prazosin, 2 mg every 8 hours (Group B, no. = 7). The plasma prazosin levels of the two groups, drawn 2 hours after administration, were 24.5 and 30.5 ng/ml, respectively. Repeated administration of prazosin in patients with congestive heart failure results in rapid attenuation of its beneficial central and regional hemodynamic effects. The usefulness of this vasodilator as a preload- and afterload-reducing agent in the clinical setting of chronic congestive heart failure may be limited by the development of pharmacodynamic tolerance.
 ...
PMID:Development of pharmacodynamic tolerance to prozosin in congestive heart failure. 49 12

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.
 ...
PMID:Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure. 49 13

Fourteen dogs with prior constriction of the left circumflex (LCf) coronary artery were studied at rest and during treadmill running. Hemodynamics were measured before and after a 1-min LCf occlusion. Coronary and collateral flows were quantitated during occlusion both at rest and during exercise. Group I consisted of 4 dogs with resting collateral flow exceeding one-half (average 78%) of normal flow, and group II consisted of 10 dogs with collateral flows less than one-half (average 30%) of normal. At rest LCf occlusion caused no hemodynamic changes in group I, but stroke volume fell significantly in group II. During running, collateral flow after LCf occlusion doubled in group I, and there was only a small rise in left atrial pressure to 18 mmHg. In group II, collateral flow increased by 50% during running and actually decreased in 4 dogs. Significant cardiac failure developed as stroke volume halved, and left atrial pressure rose to an average 30 mmHg. Therefore exercise-induced depression of left ventricular function in the ischemic heart can be correlated to the amount of coronary collateral flow.
 ...
PMID:Myocardial performance and collateral flow after transient coronary occlusion in exercising dogs. 49 38

Optimal therapy for congestive cardiac failure requires identification of correctable factors that aggravate it as well as an understanding of its etiology. Increased sympathetic nervous system activity, reduced renal blood flow, and cardiac hypertrophy and dilation are the main compensatory processes that occur in response to cardiac failure. Although they may be of initial benefit in supporting a reduced stroke volume, they may ultimately prove self-defeating. New drugs for the treatment of severe congestive heart failure include dopamine, which has a selective nonadrenergic dilator effect on the renal vascular bed, and dobutamine, which has potent inotropic effects, lowers the left ventricular filling pressure and does not increase the heart rate or the systemic vascular resistance. By reducing both the resistance to left ventricular ejection and the venous return to the right heart, vasodilators result in improved peripheral perfusion and reduced pulmonary congestion. Optimal therapy for refractory cardiac failure can be rationally determined by characterizing the hemodynamic profile through measurement of the mean arterial pressure, the left ventricular filling pressure, the cardiac output and the systemic vascular resistance. The specific therapy can then be effectively and safely delivered by a careful analysis of the dose-response relation as identified by hemodynamic monitoring.
 ...
PMID:Contributions of hemodynamic monitoring to the treatment of chronic congestive heart failure. 49 82

The effect of pentaformilgitoxin and deslanoside on heart rate, blood pressure and cardiac output was compared in six patients with heart failure. Pentaformilgitoxin caused an increase of cardiac output from 3361 ml/min to 4183 ml/min (p less than 0.01). Deslanoside induced a non significant increase of cardiac output from 3617 to 3848 ml/min. Heart rate decreased significantly by both drugs: the reduction was greater after deslanoside (from 93.7 to 77.5 beats/min) than after pentaformilgitoxin (from 92 to 85 beats/min). Both drugs caused a comparable increase in stroke volume.
 ...
PMID:Comparison of hemodynamic effects induced by pentaformilgitoxin and deslanoside in patients with heart failure. 50 Feb 57


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>