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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of mechanical ventilation with and without positive end-expiratory pressure (PEEP) on hemodynamic performance and blood-gas exchange were studied in ten patients following open-heart surgery. Ventilation at constant tidal volume (15 ml/kg body weight) with 10 cm H2O PEEP following aortic valve replacement (AVR) IN FIVE PATIENTs without pulmonary vascular disease was associated with the following significant changes: a rise in arterial Po2, a fall in the alveolar-arterial Po2 gradient when Fio2 = 1.0, decreases in calculated Qs/Qt and cardiac index. Using a similar pattern of ventilation following mitral valve replacement (MVR) in patients with elevated pulmonary vascular resistance, we found a significant decrease in cardiac index (but less than in the AVR group), a significant elevation of calculated physiologic deadspace (Vd/Vt) and no change in Qs/Qt. An hour after removal of PEEP, intravascular pressures, blood flow and blood-gas exchange values of all patients with AVR had returned to control levels; patients with MVR had persistently significantly low cardiac indices, while Vd/Vt returned to pre-PEEP values. These findings suggest that evaluation of responses to different ventilation patterns must take into account pre-existing V/Q abnormalities secondary to pulmonary vascular disease, particularly when these are secondary to chronic congestive heart failure. Following AVR, Qs/Qt changed in the same direction as cardiac index (CI) irrespective of ventilatory pattern: CI decreased and rose as CI increased. The authors conclude that with increasing severity of pulmonary vascular disease, changes in airway pressure will have an unpredictable effect on cardiac index unless the level of myocardial competence is taken into account. In the presence of ventricular failure, changes in pleural (and therefore transmural) pressures will be minimal compared with the high filling pressures and exert no influence on stroke volume. Although pulmonary venous hypertension was more pronounded in the MVR than in the AVR group, there was no significant difference between the postoperative values for Qs/Qt (Fio2 = 1.0), a condition probably fostered by marked differences in pre-existing V/Q.
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PMID:The effect of pre-existing pulmonary vascular disease on the response to mechanical ventilation with PEEP following open-heart surgery. 23 11

The Starling relationship in the normal human ventricle may be different than usually portrayed. In normal, resting, supine man the ventricular function curve is at its peak at a left ventricular end-diastolic pressure of approximately 10 mm Hg. Below this point is a strong direct relation between filling pressure and stroke work, while at higher filling pressures, a plateau occurs. Limitation of ventricular response is related to a sharply rising ventricular pressure-volume curve at a normal level of filling pressure. Thus, in the supine position, the normal heart is not on the active portion of the ventricular function curve, but is in a unique position in which cardiac output is probably controlled by factors other than ventricular filling pressure. In ventricular failure, the peak of the ventricular function curve is displaced to a higher level.
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PMID:Normal left ventricular function. 37 77

The effects of the positive-inotropic drug Canrenoat-Kalium (CRK) on the extent and severity of myocardial ischemic injury and on hemodynamic parameters were studied in 17 dogs following coronary occlusion. Acute myocardial infarction causes depression of left-ventricular function. There eas a significant decrease in dp/dtmax, stroke volume and cardiac output; average values for mean arterial pressure were reduced, but not significantly. There was a significant increase in left-ventricular enddiastolic pressure. Heart rate was unchanged. In the healing phase of myocardial infarction a significant elevation of left-ventricular enddiastolic pressure and a significant decrease of arterial pressure persisted, but the other parameters had returned toward normal. Intravenous administration of CRK (20 mg/kg) one hour after coronary occlusion causes a significant increase in left-ventricular dp/dtmax, cardiac output and stroke volume, but no significant change in arterial pressure, heart rate and left-ventricular enddiastolic pressure. Four days after myocardial infarction administration of CRK causes also a significant incrrease in left-ventricular dp/dtmax and -n 4 out of 5 animals an increase in stroke volume. Heart rate, arterial pressure and left-ventricular enddiastolic pressure are unchanged. There is a continuous deterioration of all hemodynamic parameters in the control group 1 hour and 96 hours after experimental myocardial infarction. This spontaneous deterioration has to be taken into consideration estimating the effect of CRK in experimental conditions. 120 epicardial electrocardiographic recordings were used to assess the extent and severity of myocardial ischemic injury. The average ST-segment elevation and the number of sites with abnormal ST-segments were significantly reduced 20 min after CRK administration. The study suggests a beneficial therapeutic role for CRK treatment of left-ventricular failure in the acute and healing phase after myocardial infarction.
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PMID:[Influence of canrenoate potassium (aldactone pro injections) on hemodynamics and myocardial ischemia in experimental myocardial infarct]. 116 92

From August 1979 through August 1991, 91 patients were supported with centrifugal mechanical ventricular assist. Major indications for its use were postcardiotomy ventricular failure (79) or as a bridge to cardiac transplantation (12). In postcardiotomy use (0.2% of all cardiac procedures), there were 54 male (68.4%) and 25 female patients (31.6%) with a mean age of 54.8 years and a mean duration of use of 3.56 days (range, 1 hour to 19 days). Forty-nine patients (62%) were successfully weaned, and 20 (25.3%) were hospital survivors. In 57 patients the device was inserted to wean from cardiopulmonary bypass, whereas in 22 it was employed later in the postoperative period because of low cardiac output or sudden arrest. Thirty-four (59.6%) of the 57 patients in the former group were weaned, and 15 (26.3%) were discharged, results similar to those in the latter group with 15 (68.2%) weaned and 5 (22.7%) discharged. Morbidity associated with use of centrifugal blood pumps included bleeding (87.3%; mean transfusion requirement, 53.2 units), renal failure (46.8%), cerebrovascular accident (12.7%), thromboembolism (12.7%), and hepatic insufficiency (12.7%). After a mean follow-up of 45.4 months (range, 2 to 142 months), 7 patients had died (35% late mortality), 1 patient is in functional class IV, and all others are in functional class I or II. Lower survival was associated with biventricular failure and renal failure but not with age or sex of the patient.
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PMID:Postcardiotomy centrifugal mechanical ventricular support. 144 87

The reported clinical use of the Sarns centrifugal pump (Sarns, Inc./3M, Ann Arbor, Mich.) as a cardiac assist device for postcardiotomy ventricular failure is limited. During a 25-month period ending November 1988, we used 40 Sarns centrifugal pumps as univentricular or biventricular cardiac assist devices in 27 patients who could not be weaned from cardiopulmonary bypass despite maximal pharmacologic and intraaortic balloon support. Eighteen men and nine women with a mean age of 60.4 years (28 to 83) required assistance. Left ventricular assist alone was used in 12 patients, right ventricular assist in 2, and biventricular assist in 13. The duration of assist ranged from 2 to 434 hours (median 45). Centrifugal assist was successful in weaning 100% of the patients. Ten of 27 patients (37%) improved hemodynamically, allowing removal of the device(s), and 5 of 27 (18.5%) survived hospitalization. Survival of patients requiring left ventricular assist only was 33.3% (4/12). Complications were common and included renal failure, hemorrhage, coagulopathy, ventricular arrhythmias, sepsis, cerebrovascular accident, and wound infection. During 3560 centrifugal pump hours, no pump thrombosis was observed. The Sarns centrifugal pump is an effective assist device when used to salvage patients who otherwise cannot be weaned from cardiopulmonary bypass. Statistical analysis of preoperative patient characteristics, operative risk factors, and postoperative complications failed to predict which patients would be weaned from cardiac assist or which would survive.
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PMID:Experience with the Sarns centrifugal pump in postcardiotomy ventricular failure. 151 45

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.
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PMID:Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts. 222 Nov 16

Since July 1985, cryopreserved homograft prostheses have been used for aortic valve replacement in 10 patients, aged 2 to 77 years, with active endocarditis. Five patients had positive bacterial cultures from excised valves, and all had clinical findings of uncontrolled infection while receiving appropriate antibiotics. Homograft valves (four) or valved conduits (six) were implanted for treatment of sepsis (6 patients), congestive heart failure (3) or recurrent emboli (1 patient), and complicating native (5 patients) or prosthetic valve (5) endocarditis. Staphylococci (6 patients), streptococci (3), and Candida (1) were infecting organisms. Preoperatively, Doppler echocardiography showed aortic regurgitation in all patients. At operation, 9 patients had gross vegetations, 9 had single or multiple abscess cavities, and 5 had pericarditis. Complex reconstruction of the aortic valve and annulus with homograft conduits was necessary in 6 patients (3 with previous aortoventriculoplasty). Two early deaths (ventricular failure, perioperative stroke) occurred. Mean follow-up of all operative survivors was 2.1 years (range, 0.6 to 3.6 years), and one late death resulted from arrhythmia. Homograft valve regurgitation increased in 1 patient, and 7 late survivors are asymptomatic. No patient has had recurrence of endocarditis. We conclude that cryopreserved homograft aortic valve/root replacement is an effective method for management of active endocarditis complicated by annular destruction.
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PMID:Results of homograft aortic valve replacement for active endocarditis. 232 58

Methods for mechanical cardiac support by intermittent increases in the intrathoracic pressure have recently been described. In the present study the responses of the arterial pressure waveform to mechanical ventilation with and without synchronized external chest compression (SEC) in the presence of acute ventricular failure (AVF) were evaluated by measuring the systolic pressure variation (SPV). SPV, the difference between the maximal and minimal values of systolic blood during a single positive pressure breath, consists of delta up and delta down components when systolic blood pressure during a short apnea is used as reference value. During intermittent positive pressure ventilation (IPPV) alone, AVF caused SPV to decrease significantly from 8.8 +/- 4.0 to 5.7 +/- 1.9 mm Hg, and further to 3.1 +/- 1.1 mm Hg after volume loading (P less than 0.02). The decrease in SPV was due to a significant decrease in the delta down component, whereas the delta up became the major component of the reduced SPV. The application of SEC caused significant increases in the delta down, delta up, and overall SPV during AVF without volume loading. However, during AVF with volume loading, SEC increased only the delta up component of the SPV, signifying a transient increase in the left ventricular stroke output. It is concluded that the disappearance of the delta down component of the SPV is characteristic of congestive heart failure. Analysis of the arterial waveform offers a readily available monitoring tool for the differentiation of the possible effects on increased intrathoracic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The arterial pressure waveform during acute ventricular failure and synchronized external chest compression. 264 88

An attempt was made to noninvasively assess the myocardial reserve by using a bimanual isometric exercise (BIE) in patients with aortic failure depending on the degree of aortic regurgitation (AR). The patients with Grade I AR, like healthy subjects, showed their responses to BIE, by significantly enhancing systolic BP, heart rate (HR), left ventricular ejection fraction (LVEF), stroke index and decreasing the end systolic volume of the left ventricle, which indicated that the left ventricle had great compensatory potentialities. With physical exercise, the patients with Grade II AR displayed an inadequately small increase in LVEF and velocity of myocardial circular fiber contractions, which suggested latent ventricular failure and was an indicator of diminished myocardial reserve. In response to BIF, there was a significant reduction in LVEF along with a substantial increase in the maximal size of the left atrium in the patients with Grade III AR, attesting that myocardial functional potentialities were considerably reduced.
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PMID:[Functional state of the left heart in aortic regurgitation of varying degrees]. 277 84

Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.
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PMID:Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure. 351 12


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