Alterations of hemostasis associated with cardiopulmonary bypass

Bick, Rodger L.; Schmalhorst, William R.; Arbegast, Neil R.

doi:10.1016/0049-3848(76)90023-2

Cited by 59 publications

(75 citation statements)

References 32 publications

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“…Results of the biological study confirmed that ECC provokes a decrease in the concen tration of several hemostatic factors [14,15], No differences were observed between the mean values obtained in the LMW, LD or HD heparin groups. The explanation for the slight decrease in fibrin, AT III, F V and AP is the combined effect of hemodilution and adsorption of these proteins on the interfaces [13,15], A moderate FDP elevation was ob served at To and during the ECC in the three groups of animals, probably as a result of sur gical procedure.…”

Section: Discussionsupporting

confidence: 55%

Low Molecular Weight (LMW) Heparin Derivatives in Experimental Extra-Corporeal Circulation (ECC)

Aiach¹,

Dreyfus

Michaud³

et al. 1984

Pathophysiol Haemos Thromb

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Low molecular weight (LMW) heparin has been shown to prevent experimental venous thrombosis. In order to investigate its biological action and its potential use in open heart surgery, we have conducted an experimental study using extracorporeal circulation (ECC) in sheep as an experimental model. 18 sheep were randomly selected to receive either LMW heparin (2 mg/kg), high dose heparin (HD; 160 U/kg), or low dose heparin (LD; 60 U/kg). The HD heparin yielded the same circulating anti-activated factor X (anti-Xa) activities as the LMW heparin and the LD heparin yielded the same anti-thrombin activity. LMW heparin and HD heparin were both effective in preventing blood clotting in the ECC circuit, demonstrating the antithrombotic activity of the LMW heparin. Clotting in the circuit was observed following LD heparin administration showing that the efficacy of LMW heparin does not only rely upon its weak anti-activated partial thromboplastin time (APTT) and antithrombin activity. Fibrinogen, fibrinogen degradation products (FDP), factor V (F V), platelet count, antithrombin III (AT III), fast acting antiplasmin (AP) were evaluated during and after ECC. The defects in hemostasis were similar in the three groups. Conclusions were: (1) heparin chain depolymerization diminishes the anti-APTT activity without altering the antithrombotic property; (2) LMW heparin is an effective alternative to heparin in cardiac surgery; (3) the absence of postoperative circulating anti-APTT activity might be associated with a reduced incidence of hemorrhagic complication, but we were not able to demonstrate it.

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Section: Discussionsupporting

confidence: 55%

Low Molecular Weight (LMW) Heparin Derivatives in Experimental Extra-Corporeal Circulation (ECC)

Aiach¹,

Dreyfus

Michaud³

et al. 1984

Pathophysiol Haemos Thromb

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“…Perfusions of the circulatory system with devices like the cardiopulmonary bypass (CPB) and CAD disturb endothelial shear stress (ESS), which is responsible for the postcardiotomy syndrome, increasing liabilities of clot formation, bleeding, disseminated syndrome, etc (Bick et al, 1976)) (Abshire, 2009). This endothelial dysfunction syndrome is most probably occurred due to steady flow, foreign surfaces and the severe momentum energy losses.…”

Section: Evaluation Of the Pulsatile Tube Devicementioning

confidence: 99%

“Flow and Rate”: Concept and Clinical Applications of a New Hemodynamic Theory

Nour¹

2012

Biophysics

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“…The hemostatic complications that accompany the insertion of prosthetic devices include activation of coagulation factors, 'consumption' of coagulation factors and other plasma proteins and platelets and the generation of microthrombi. Also, life-threatening thrombosis or thromboembolism may de- velop in those with prosthetic devices [2][3][4][5]60]. Intra-aortic balloon assist devices may activate the coagulation system with an attendant low-grade DIC, which may become fulminant [3].…”

Section: Etiologymentioning

confidence: 99%

“…Intra-aortic balloon assist devices may activate the coagulation system with an attendant low-grade DIC, which may become fulminant [3]. LeVeen or Denver valve shunting for peritoneovenous or pleurovenous shunting is a common palliative procedure and generalized DIC is often seen with the use of these shunts [2,3,60,61]. The removal of ascitic fluid at the time of LeVeen or Denver valve implantation, and the use of low-dose heparin may abort DIC [2][3][4][5].…”

Section: Etiologymentioning

confidence: 99%

Disseminated Intravascular Coagulation

Bick¹,

Arun²

1999

Pathophysiol Haemos Thromb

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Disseminated intravascular coagulation (DIC) is a complex disorder, with pathophysiology being variable and highly dependent upon the triggering event(s), host response(s) and comorbid conditions. As a result of these complicated interactions, the clinical expression and laboratory findings are varied, thereby affecting the specifics of diagnosis and therapeutic approaches. The highly complex and variable pathophysiology of DIC often results in a lack of uniformity in clinical manifestations, a lack of consensus in the specific appropriate laboratory criteria of diagnosis, and a lack of specific therapeutic modalities. Indeed, recommendations for therapy are often difficult because the morbidity and survival is more dependent on the specific cause of DIC and because the generally used specific therapeutic approaches, which include for example heparin, low-molecular-weight-heparin antithrombin concentrate and protein C concentrate, have never been subjected to objective prospective randomized trials, except antithrombin concentrates. An analysis of the complex and varied pathophysiological events in DIC provide objective guidelines and criteria for the clinical diagnosis, the laboratory diagnosis, and the definition of severity. These data compounded by an understanding of complex and varied pathophysiology can be used for objective evaluation of therapeutic responses and results. DIC is an intermediary mechanism of disease usually seen in association with well-defined clinical disorders. The pathophysiology of DIC serves as an intermediary mechanism in many disease processes, which sometimes remain organ specific. This catastrophic syndrome spans all areas of medicine and presents a broad clinical spectrum that is confusing to many. Most physicians consider DIC to be a systemic hemorrhagic syndrome; however, this is only because hemorrhage is evident and often impressive. Less commonly appreciated is the profound microvascular thrombosis and sometimes, large vessel thrombosis. The hemorrhage is often simple to contend with in patients with fulminant DIC, but it is the small- and large-vessel thrombosis, with impairment in blood flow, ischemia, and associated end-organ damage that usually leads to irreversible morbidity and mortality. In conclusion, the pathophysiological mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents which can block, blunt or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending o...

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Alterations of hemostasis associated with cardiopulmonary bypass

Cited by 59 publications

References 32 publications

Low Molecular Weight (LMW) Heparin Derivatives in Experimental Extra-Corporeal Circulation (ECC)

Low Molecular Weight (LMW) Heparin Derivatives in Experimental Extra-Corporeal Circulation (ECC)

“Flow and Rate”: Concept and Clinical Applications of a New Hemodynamic Theory

Disseminated Intravascular Coagulation

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