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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-four consecutive patients with acute myocardial infarction were studied with equilibrium radionuclide angiography (RNA) within 24 hours from the onset of symptoms, three days after admission and three days before hospital discharge (14 +/- 3 days). To assess the prognostic value of RNA derived parameters we assessed: the ejection fraction (EF), the left ventricular end-systolic volume index (ESVI), the left ventricular end-diastolic volume index (EDVI), the cardiac index (CI), the stroke volume index (SVI) and the peak systolic pressure/end-systolic volume index ratio (PSP/ESVI); we also determined Peel's prognostic index (PI) on admission and measured systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and cardiac frequency (CF) as the same time as the radioisotopic parameters were taken. Thirty-nine patients were discharged without signs of ventricular failure with and without medical treatment (group A), 5 died during hospitalization (group B). Using EF alone, we obtained a very clear distinction between the two groups (Group A 43 +/- 12%; Group B 22 +/- 3%; p less than 0.005). Stepwise, multivariate analysis showed that, by linking PSP/ESVI to EF, we can even obtain a function that correlate better with hospital survival (F = 0.09832 X EF - 0.32035 X PSP/ESVI - 3.12981; p less than 0.002). There was good exponential correlation between EF and PSP/ESVI (r = 0.781) and this would seem to confirm that PSP/ESVI is a more sensitive contractility index for patients with a not very depressed EF.
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PMID:[Prognostic setting and bloodless hemodynamic evaluation of acute myocardial infarct with equilibrium radioisotopic ventriculography]. 373 24

We define matching between ventricle and afterload to imply that the ventricle is adapted to its afterload to yield maximum external work output. For the ventricle, this optimal adaption will depend on end-diastolic dimension, heart rate, and contractility. Because contractility is impaired during ventricular failure, we propose that the adaption between ventricle and load is not as good during failure as during normal conditions. According to our definition, this implies that during failure external work output is less than maximum. Ventricle-load matching is then not present, i.e., a mismatch exists between ventricle and load. This hypothesis was tested in a canine preparation in which arterial load of the left ventricle was varied from one beat to the next. Left ventricular depression was induced by injections of 50 micron microspheres into the left coronary bed. We observed left ventricular stroke volume and external work during afterload variations at three different preload levels before and after microembolization. Before embolization the control observations of work and stroke volume were positioned at the apex of parabolas relating work to stroke volume. After embolization, however, control observations fell down along the left limb of the parabolas. These observations were independent of preload. Thus this study, carried out in a preparation with the heart in situ, supports the idea that the normal left ventricle is matched to its load and demonstrates ventricle-load mismatch when the left ventricle is failing.
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PMID:The effect of contractility and preload on matching between the canine left ventricle and afterload. 375 86

We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. We found that pertubations in mean ITP induced by ventilator adjustments accounted for all observable steady-state hemodynamic changes independent of respiratory frequency, inspiratory time, or phasic respiratory swings in ITP. Changes in ITP were associated with reciprocal changes in both intrathoracic vascular pressures (P less than 0.01) and blood volume (P less than 0.01). When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.
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PMID:Determinants of cardiac augmentation by elevations in intrathoracic pressure. 398 74

Hemodynamic and ECG effects of intravenous flecainide were assessed in 10 patients with acute myocardial infarction and no symptoms or signs of heart failure. The dose was 2 mg/kg injected over a 15-minute period. R-R interval did not change, but PR interval and QRS increased significantly, 28% (p less than 0.0005) and 20% (p less than 0.05), respectively. Duration of P wave also increased significantly, 15% (p less than 0.02). Pulmonary wedge pressure increased 29% (p less than 0.005) and cardiac index and left ventricular stroke work index decreased 9% (p less than 0.05) and 20% (p less than 0.05), respectively. No significant change in mean aortic pressure and systemic vascular resistance occurred. Thus, intravenous flecainide has a mild and transient negative inotropic effect in patients with noncomplicated acute myocardial infarction. It did not induce ventricular failure in this group of patients but should be administered cautiously to patients with overt heart failure or severe conduction defects.
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PMID:Hemodynamic effects of intravenous flecainide in acute noncomplicated myocardial infarction. 407 76

Ten patients with moderate to severe congestive heart failure (CHF) underwent central and regional hemodynamic measurements at rest and central hemodynamic measurements during exercise before and after the oral administration of nifedipine (0.2 mg/kg). Nifedipine significantly decreased systemic blood pressure, systemic vascular resistance, pulmonary artery pressure, pulmonary vascular resistance, and pulmonary capillary wedge pressure. Stroke volume and cardiac output increased after nifedipine. The measured parameters of left ventricular inotropy did not change significantly for this calcium channel blocker. While blood flow to renal, hepatic, and limb vascular beds increased (p less than 0.05 for renal and limb) after nifedipine, only limb blood flow increased in proportion to the increase in cardiac output, suggesting preferential dilatation of limb vasculature. Although initial-dose nifedipine did not increase exercise duration, it elicited an improvement in exercise hemodynamics by reducing systemic vascular resistance and pulmonary capillary wedge pressure and increasing stroke volume and cardiac output. The calcium channel blocker, nifedipine, can be administered safely in the setting of ventricular failure and appears to favorably alter resting and exercise hemodynamics. A select number of patients with CHF may benefit from its long-term administration.
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PMID:Nifedipine in congestive heart failure: effects on resting and exercise hemodynamics and regional blood flow. 650 42

The hemodynamic effects induced by an i.v. administration of Amiodarone (5 mg/Kg in 10 min + continuous infusion of 0.6 mg/min for 4-40 hrs), Propafenone (1-2 mg/Kg in 5 min + continuous infusion of 10-15 mcg/Kg/min for 24 hrs) and Mexiletine (250 mg in 15 min + 250 mg in 1 hr) have been evaluated in patients with acute myocardial infarction complicated by sinus tachycardia and hyperdynamic pattern, ventricular or supraventricular arrhythmias. The hemodynamic serial determinations have been comprehensive of: heart rate; systolic, diastolic and mean pressure; central venous pressure; arterial and wedge pulmonary pressure; cardiac output and cardiac index; vascular systemic resistences; left ventricular stroke work index; left ventricular mean ejection rate; double and triple product. In all of the three groups we observed: a reduction of cardiac index associated with an increase of left and right ventricular filling pressure and a reduction either of left ventricular stroke work index and left ventricular mean ejection rate; these hemodynamic changes were less significant after Mexiletine than after Amiodarone or Propafenone. These data confirm the negative inotropic effect of the three drugs; anyhow, these changes are usually well tolerated by patients affected by AMI with a sufficiently preserved ventricular function. The authors, however, reccommend an accurate hemodynamic monitoring of the effects of the drugs also to identify patients with a not overt ventricular failure which may become manifest after drug administration.
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PMID:Hemodynamic effects of antiarrhythmic drugs in acute myocardial infarction. 651 85

The so-called safe course of acute myocardial infarction was shown to be associated with reduced left ventricular stroke output, changed phasic pattern of the systole, and peripheral arterial constriction. In infarction-related acute left-ventricular failure, a clear dissociation can be seen between the pumping function of the right and left ventricles. These changes are further aggravated by increased circulating blood volume and pulmonary blood quantity, and lowered arterial and venous flow rate. Paravascular edema adds to generalized vasoconstriction. Hypertension in the pulmonary artery network implies additional effort for right ventricular myocardium and thus prevents blood overflow to lesser circulation veins and left compartments of the heart.
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PMID:[Comparative hemodynamic aspects in acute myocardial infarctions with various clinical patterns]. 662 Aug 7

Data were collected from 17 patients with valvular regurgitation and ventricular failure who were about to undergo prosthetic replacement of an insufficient cardiac valve. Awake control hemodynamic measurements revealed that these patients came to the operating room with a high systemic vascular resistance of 38 units and low cardiac and stroke volume indices of 2.2 L/min/m2 and 30 ml/beat/m2, respectively. A preanesthetic infusion of nitroprusside together with almost 2 L of lactated Ringer's solution caused vascular resistance to decrease to 19 units (normal) while filling pressure remained high. As a result, while the combined therapy continued, neither the induction of anesthesia nor surgical stimulation produced cardiovascular deterioration; in fact, cardiac index measured above 3.1 L/min/m2 and stroke volume index above 40 ml/beat/m2 throughout anesthesia and surgery. We conclude, therefore, that the combination of afterload reduction and preload augmentation provides the best possible environment within which to conduct the anesthetic management of patients with valvular regurgitation and ventricular failure.
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PMID:Afterload reduction and preload augmentation improve the anesthetic management of patients with cardiac failure and valvular regurgitation. 719 46

Left dominant biventricular failure is a common type of heart failure after cardiac surgery. We developed a biventricular bypass (BVB) system for treatment of postcardiotomy ventricular failure, and we previously reported that the clinical results of the BVB system were superior to those obtained with venoarterial bypass (VAB). The purpose of this study was to evaluate the effect of the BVB system on left ventricular (LV) performance in comparison to that of VAB by means of the LV pressure-volume relationship (PVR). Eight adult mongrel dogs (14-21 kg) underwent VAB with right atrial and aortic cannulation. Left atrial cannulation was added for BVB, and both atrial drainage tubes were joined with a Y-shaped connector. The bypass flow was maintained at half of the baseline cardiac output (0.7-1.0 L/min), and the hemodynamic parameters were monitored. A high fidelity microtip catheter and a conductance catheter were used to evaluate LV function. The slope of the LV end-systolic pressure-volume relation (Emax), the slope of the LV end-systolic pressure-stroke-volume relation (Ea), the LV stroke work (SW), LV potential energy (PE), LV pressure-volume area (PVA), the slope of the SW end-diastolic volume relation (PRSW), and an index of the LV energizing charge (ratio of PE/PVA) were assessed during transient occlusion of the inferior vena cava. LV contractility (Emax) showed no significant change during each experiment. Standardized LV work (PRSW) was reduced by BVB in comparison to the baseline and in comparison to VAB. The rate of LV energy charge (PE/PVA) significantly increased only during BVB. These results suggested that the BVB system might be an effective circulatory support for reducing LV work and improving the LV energizing charge in patients with severe heart failure after cardiac operation.
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PMID:Effect of a balanced biventricular bypass system on left ventricular energies. 975 70

The cardiovascular, coagulation and haematological effects of prothrombin activator from Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized mechanically ventilated dogs. Infusion caused dose-related systemic hypotension, marked decreases in cardiac output and stroke volume, marked increases in pulmonary artery pressure, pulmonary artery occlusion pressure and pulmonary vascular resistance. Effects occurred within several minutes but abated over 30 to 40 minutes. Evidence of procoagulation included prolongation of prothrombin and partial thromboplastin times and depletion of serum fibrinogen. Thrombocytopenia and leucopenia occurred. All effects were prevented by prior administration of heparin but none by inhaled nitric oxide. Oesophageal echocardiography during infusion identified thrombi within the heart, right ventricular dilatation and dyskinesia. Electrocardiography suggested myocardial ischaemia. Pulmonary thromboemboli were identified histologically post mortem. Cardiovascular effects of the activator were not due to a variety of endogenous substances as indicated by use of antagonists to platelet activating factor and thromboxane A2 indomethacin, dexamethasone, serotonin, ketanserin, histamine, promethazine and ondansetron. Tiger Snake prothrombin activator causes bilateral ventricular failure by thrombotic obstruction of the pulmonary vasculature and possibly by coronary ischaemia.
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PMID:The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) prothrombin activator and investigation of release of vasoactive substances. 980 10


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