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Hemodynamic Abnormalities (hemodynamic + abnormality)
Selected AbstractsReliability of Intraoperative Transesophageal Echocardiography During Tetralogy of Fallot RepairECHOCARDIOGRAPHY, Issue 4 2000JAMES J. JOYCE M.D. There is limited information available concerning the accuracy of intraoperative transesophageal echocardiography (TEE) in predicting the extent of residual abnormalities after recovery from surgical repair of tetralogy of Fallot. Therefore, we investigated differences between the results of final postbypass TEE and those of postrecovery (mean, 6 days after surgery) transthoracic echocardiography in a total of 28 consecutive pediatric patients who underwent repair of tetralogy of Fallot with biplane or multiplane TEE. Both postbypass and postrecovery echocardiographic examinations included measurements of the right ventricle (RV)-main pulmonary artery (PA) and the main PA-branch PA peak instantaneous gradients, the degree of pulmonary valvar insufficiency, and color Doppler interrogation of the ventricular septum for residual defects. The RV-main PA gradient did not change significantly: 15 ± 13 vs 18 ± 14 mmHg (postbypass versus postrecovery, mean ± SD). None of the patients had a decrease of , 10 mmHg; and only one patient had an increase of ,: 15 mmHg. There also was no change in the degree of pulmonary insufficiency (3.0 ±1.2 versus 3.1 ± 1.1, using a scale of 0 to 4). Only one of the seven very small (, 2 mm) residual ventricular septal defects was not discovered during postbypass TEE. However, postrecovery transthoracic echocardiography detected significant branch PA stenosis (peak gradient, , 15 mmHg) in five patients (18%) that was not detected during postbypass TEE (P < 0.03). Of the branch PA stenoses that were not detected during TEE, four were left and one was right. Conclusions: Postbypass TEE after tetralogy of Fallot repair reliably predicts residual postrecovery hemodynamic abnormalities, except for branch PA stenosis. [source] Application of intensive care medicine principles in the management of the acute liver failure patientLIVER TRANSPLANTATION, Issue S2 2008David J. Kramer Key Points 1Acute liver failure is a paradigm for multiple system organ failure that develops as a consequence of sepsis. 2In the United States, systemic inflammatory response, sepsis, and septic shock are common reasons for intensive care unit admission. Intensive care management of these patients serves as a template for the management of patients with acute liver failure. 3Acute liver failure is attended by high mortality. Although intensive care results in improved survival, the key treatment is liver transplantation. Intensive care unit intervention may open a "window of opportunity" and enable successful liver transplantation in patients who are too ill at presentation. 4Intracranial hypertension complicates the course for many patients with acute liver failure. Initially, intracranial hypertension results from hyperemia, which is cerebral edema that reduces cerebral blood flow and eventuates in herniation. The precepts of neurocritical care,monitoring cerebral perfusion pressure, cerebral blood flow, and cortical activity,with rapid response to hemodynamic abnormalities, maintenance of normoxia, euglycemia, control of seizures, therapeutic hypothermia, osmotic therapy, and judicious hyperventilation are key to reducing mortality attributable to neurologic failure. Liver Transpl 14:S85,S89, 2008. © 2008 AASLD. [source] Rapid clinical assessment of hemodynamic profiles and targeted treatment of patient with acutely decompensated heart failureCLINICAL CARDIOLOGY, Issue S5 2004Greegg C. Fonarow M.D. Abstract Acutely decompensated heart failure (ADHF) is characterized by hemodynamic abnormalities and neurohormonal activation that contribute to heart failure (HF) symptoms, end-organ dysfunction, arrhythmias, and progressive cardiac failure. The management of ADHF in the emergency department (ED) can be simplified and improved by a 2-min bedside assessment that identifies any of four possible hemodynamic profiles on the basis of clinical signs and symptoms. The profiles are based on whether congestion is present or absent (wet or dry) and perfusion is adequate or limited (warm or cold). A wet-warm profile is seen more frequently in the ED than any of the other three profiles (wet-cold, dry-warm, and dry-cold). The four clinically determined profiles have been shown to predict clinical outcomes and may be used to guide initial HF therapy. The goals of treating ADHF are to stabilize the patient, reverse acute hemodynamic abnormalities, rapidly reverse dyspnea and/or hypoxemia caused by pulmonary congestion, and initiate treatments that will decrease disease progression and improve survival. An ideal agent for the wet-warm profile would rapidly reduce pulmonary congestion, produce balanced arterial and venous dilation, promote natriuresis, lack direct positive inotropic effects, and not cause reflex neuroendocrine activation. Intravenous nesiritide in conjunction with loop diuretics has been found safe and effective as initial treatment for patients with the wet-warm profile. For the wet-cold profile, more intensive therapy and invasive hemodynamic monitoring may prove useful. This review will discuss the rapid clinical determination of hemodynamic profiles in patients presenting to the ED with ADHF and the options for their initial medical management. Case studies representing the wet-warm, wet-cold, dry-warm, and dry-cold profiles will be presented and discussed. [source] Rest and exercise hemodynamics before and after valve replacement-A combined doppler/catheter studyCLINICAL CARDIOLOGY, Issue 1 2000G. Inselmann M.D. Abstract Background: Hemodynamic improvement is a common finding following valve replacement. However, despite a normally functioning prosthesis and normal left ventricular ejection fraction, some patients may show an abnormal hemodynamic response to exercise. Methods: In a combined catheter/Doppler study, rest and exercise hemodynamics were evaluated in 23 patients following aortic (n = 12) (Group 1) or mitral valve (n = 11) (Group 2) replacement and compared with preoperative findings. Patient selection was based on absence of coronary artery disease and left ventricular failure as shown by preoperative angiography. Cardiac output, pulmonary artery pressure, pulmonary capillary pressure, and pulmonary resistance were measured by right heart catheterization, whereas the gradient across the valve prosthesis was determined by Doppler echocardiography. Postoperative evaluation was done at rest and during exercise. The mean follow-up was 8.2 ± 2.2 years in Group 1 and 4.2 ± 1 years in Group 2. Results: With exercise, there was a significant rise in cardiac output in both groups. In Group 1, mean pulmonary pressure/capillary pressure decreased from 24 ± 9/18 ± 9 mmHg preoperatively to 18 ± 2/12 ± 4 mmHg postoperatively (p < 0.05), and increased to 43 ± 12/30 ± 8 mmHg with exercise (p < 0.05). The corresponding values for Group 2 were 36 ± 12/24 ± 6 mmHg preoperatively, 24 ± 7/17 ± 6 mmHg postoperatively (p < 0.05), and 51 ± 2/38 ± 4 mmHg with exercise (p < 0.05). Pulmonary vascular resistance was 109 ± 56 dyne·s·cm -5 preoperatively, 70 ± 39 dyne·s·cm -5 postoperatively (p < 0.05), and 70 ± 36 dyne·s·cm -5 with exercise in Group 1. The corresponding values for Group 2 were 241 ± 155 dyne·s·cm -5, 116 ± 39 dyne·s·cm -5 (p < 0.05), and 104 ± 47 dyne·s·cm -5. There was a significant increase in the gradients across the valve prosthesis in both groups, showing a significant correlation between the gradient at rest and exercise. No correlation was found between valve prosthesis gradient and pulmonary pressures. Conclusion: Exercise-induced pulmonary hypertension and abnormal left ventricular filling pressures seem to be a frequent finding following aortic or mitral valve replacement. Both hemodynamic abnormalities seem not to be determined by obstruction to flow across the valve prosthesis and may be concealed, showing nearly normal values at rest but a pathologic response to physical stress. [source] | ||||||||||