			Home About us Contact

Hemodynamic Support (hemodynamic + support)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Coronary no-reflow phenomenon: From the experimental laboratory to the cardiac catheterization laboratory,

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 7 2008
Shereif H. Rezkalla MD
Abstract Coronary no-reflow occurs commonly during acute percutaneous coronary intervention, particularly in patients with acute myocardial infarction and those with degenerated vein grafts. It is associated with a guarded prognosis, and thus needs to be recognized and treated promptly. The pathophysiology originates during the ischemic phase and is characterized by localized and diffuse capillary swelling and arteriolar endothelial dysfunction. In addition, leukocytes become activated and are attracted to the lumen of the capillaries, exhibit diapedesis and may contribute to cellular and intracellular edema and clogging of vessels. At the moment of perfusion, the sudden rush of leukocytes and distal atheroemboli further contributes to impaired tissue perfusion. Shortening the door-to-balloon time, use of glycoprotein IIb/IIIa platelet receptor inhibitors and distal protection devices are predicted to limit the development of no-reflow during percutaneous interventions. Distal intracoronary injection of verapamil, nicardipine, adenosine, and nitroprusside may improve coronary flow in the majority of patients. Hemodynamic support of the patient may be needed in some cases until coronary flow improves. © 2008 Wiley-Liss, Inc. [source]

Extended Mechanical Circulatory Support With a Continuous-Flow Rotary Left Ventricular Assist Device

CONGESTIVE HEART FAILURE, Issue 2 2010
Scott Harris DO
Background LVAD therapy is an established treatment modality for patients with advanced heart failure. Pulsatile LVADs have limitations in design precluding their use for extended support. Continuous-flow rotary LVADs represent an innovative design with potential for small size and greater reliability by simplification of the pumping mechanism. Methods In a prospective multicenter study, 281 patients urgently listed (United Network for Organ Sharing status 1A or 1B) for heart transplant underwent implant of a continuous-flow LVAD. Survival and transplant rates were assessed at 18 months. Patients were assessed for adverse events throughout the study and for quality of life, functional status, and organ function for 6 months. Results Of 281 patients, 222 (79%) underwent transplant or LVAD removal for cardiac recovery or had ongoing LVAD support at 18-month follow-up. Actuarial survival on support was 72% (95% confidence interval, 65%,79%) at 18 months. At 6 months, there were significant improvements in functional status and 6-minute walk test results (from 0% to 83% of patients in New York Heart Association functional class I or II and from 13% to 89% of patients completing a 6-minute walk test) and in quality of life (mean values improved 41% with Minnesota Living With Heart Failure and 75% with Kansas City Cardiomyopathy questionnaires). Major adverse events included bleeding, stroke, right heart failure, and percutaneous lead infection. Pump thrombosis occurred in 4 patients. Conclusions A continuous-flow LVAD provides effective hemodynamic support for at least 18 months in patients awaiting transplant, with improved functional status and quality of life. [source]

The Role of Intra-Aortic Counterpulsation in High-Risk OPCAB Surgery:

JOURNAL OF CARDIAC SURGERY, Issue 4 2003
A Prospective Randomized Study
This prospective and randomized study evaluates the efficacy and safety of pre- and perioperative IABC in high-risk OPCAB. Material: Group A,IABC started prior to induction of anesthesia (n = 15); group B,no preoperative IABC (n = 15). Adult high-risk coronary patients to undergo OPCAB. High risk = (minimum 2) EF < 0.30, left main stenosis, unstable angina, redo. Bailout if hemodynamic instability CPB or IABC in group B. Study endpoints (a) cardiac protection (troponin 1, cardiac index (CI), ECG), (b) inflammatory response (lactate, IL-6), (c) clinical outcome (mortality, morbidity). Emergency operations 33%, re-operation 13%, unstable angina 100%, left main 60% and EF 0.29, without group differences. Results: No bailout group A, 10 in group B, p < 0.0001. Postoperative IABC six (group A) and seven patients (group B), during 6.8 ± 5.1 hours (group A) versus 41.2 ± 25.5 hours (group B), p = 0.0110. Myocardial protection without group differences, but CI significantly better in group A. Inflammatory response significantly less in group A. Clinical outcomes: one death, one MI and two renal failure in group B, none in group A. Intensive care unit (ICU) stay 27 ± 3 hours (group A) versus 65 ± 28 hours (group B), p = 0.0017. LOS 8 ± 2 days (group A) versus 15 ± 10 (group B), p = 0.0351. No IABC related complications. Conclusions: Pre- and perioperative IABC therapy offers efficient hemodynamic support during high-risk OPCAB surgery, lowers the risk of hemodynamic instability, is safe and shortens both ICU and hospital length of stay significantly, and is a cost-effective therapy. (J Card Surg 2003; 18:286-294) [source]

Life threatening medullary injury following adenoidectomy and local anesthetic infiltration of the operative bed

PEDIATRIC ANESTHESIA, Issue 2 2009
ELI HERSHMAN MD
Summary Objective:, To draw attention to a rare, life threatening complication of a rather common procedure, namely medullary injury following adenoidectomy and local anesthetic infiltration of the operative bed. Design:, Case report. Setting:, A tertiary pediatric critical care unit. Patient:, A healthy 7-year-old girl underwent adenoidectomy and local anesthetic infiltration of the adenoid bed with lidocaine and adrenaline. In the recovery room, nystagmus, dysarthria, dyspnea, inability to cough and right hemiparesis were noticed. Because of her inability to remove secretions tracheal intubation was performed, followed by severe, life threatening respiratory failure. Interventions:, Tracheal intubation, hemodynamic support, prolonged mechanical ventilation, nitric oxide, and tracheostomy. Conclusion:, In children, local anesthetic infiltration of the adenoid bed may cause life-threatening medullary injury and its routine use should be re-considered. [source]

Percutaneous ex-vivo femoral arterial bypass: A novel approach for treatment of acute limb ischemia as a complication of femoral arterial catheterization

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2006
William M. Merhi DO
Abstract This report describes the use of a percutaneous ex-vivo femoral arterial bypass in three patients with acute lower extremity ischemia that occurred as a complication of femoral artery catheterization. Utilizing standard equipment and techniques, a percutaneous ex-vivo femoral artery bypass can restore antegrade flow to the ischemic limb in patients with impaired aorto-iliac inflow circulation, which may arise from iatrogenic dissection or the need for large in-dwelling sheaths required for hemodynamic support. This technique is considered a temporizing measure when conventional therapies are not possible. Contrast angiography is recommended to localize and define the cause of limb ischemia, and to permit safe placement of vascular sheaths in the "donor and recipient" arteries. © 2006 Wiley-Liss, Inc. [source]

Inotropes in the beta-blocker era

CLINICAL CARDIOLOGY, Issue S3 2000
B. D. Lowes M.D.
Abstract Beta-adrenergic blocking agents are now standard treatment for mild to moderate chronic heart failure (CHF). However, although many subjects improve on beta blockade, others do not, and some may even deteriorate. Even when subjects improve on beta blockade, they may subsequently decompensate and need acute treatment with a positive inotropic agent. In the presence of full beta blockade, a beta agonist such as dobutamine may have to be administered at very high (> 10 ,g/kg/min) doses to increase cardiac output, and these doses may increase afterload. In contrast, phosphodiesterase inhibitors (PDEIs) such as milrinone or enoximone retain their full hemodynamic effects in the face of beta blockade. This is because the site of PDEI action is beyond the beta-adrenergic receptor, and because beta blockade reverses receptor pathway desensitization changes, which are detrimental to PDEI response. Moreover, when the combination of a PDEI and a beta-blocking agent is administered long term in CHF, their respective efficacies are additive and their adverse effects subtractive. The PDEI is administered first to increase the tolerability of beta-blocker initiation by counteracting the myocardial depressant effect of adrenergic withdrawal. With this combination, the signature effects of beta blockade (a substantial decrease in heart rate and an increase in left ventricular ejection fraction) are observed, the hemodynamic support conferred by the PDEI appears to be sustained, and clinical results are promising. However, large-scale placebo-controlled studies with PDEIs and beta blockers are needed to confirm these results. [source]