Masters Degrees (Anaesthesiology and Critical Care)
Permanent URI for this collection
Browse
Browsing Masters Degrees (Anaesthesiology and Critical Care) by Subject "Cardiopulmonary bypass"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
- ItemThe ability of the thromboelastogram (TEG® R-time difference between kaolin and heparinase) as a point of care test to predict residual heparin activity after in vitro protamine titration(Stellenbosch : Stellenbosch University, 2017-12) Joseph, Lauren Ann; Levin, Andrew I.; Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Anaesthesiology and Critical Care.ENGLISH ABSTRACT: Background: Differentiation between surgical bleeding and coagulopathy is critical as re-exploration is associated with increases in mortality and morbidity. Adequate reversal of heparin with protamine at the end of cardiopulmonary bypass (CPB) is critical to prevent postoperative bleeding. Meticulous dosing of protamine is required as excessive dosages has deleterious side effects on clotting. Traditional methods make use of an activated clotting time (ACT) for evaluation of adequate heparin reversal. However, recent use of other point of care (POC) tests, the thromboelastogram (TEG®) has started challenging the utility and exclusive use of ACT to evaluate effective reversal. Differences between thromboelastographic Rkaolin and R-heparinase times is an indicator of residual heparin. However, the exact relationship between these parameters and the exact amount of residual heparin is unknown. The rationale for this study was to accurately determine the relationship between the magnitude of the R-kaolin and R-heparinase time difference and blood heparin concentrations. Aims: This study was performed to define the in-vitro relationship between the difference between the thromboelastographic R-kaolin and R-heparinase time difference (TEG® Delta-kh R-time) and plasma heparin concentrations. The primary outcome was to determined the relationship between the TEG® Delta-kh R-time difference and heparin concentrations. The secondary outcome was to determine the concentration of heparin at or below which R-kaolin times become measureable. Methods: This was a single centre, prospective, randomized laboratory study. Following institutional ethics approval and informed consent, sixty-two samples were taken during CPB from 20 patients meeting inclusion criteria. Samples were randomized to one of three groups which would dictate the protamine dose. The three groups were based on a protamine to heparin ratio (expressed as milligram protamine per milligram heparin administered to the patient) approximating 0.25, 0.5, and 0.75 mg/mg respectively. Each sample of blood was then administered a dose of protamine. The TEG® analysis entailed measuring the R-kaolin and R-heparinase time and noting the difference. Thereafter, each blood sample was sent for heparin concentration determination using an anti-Xa activity assay. Results: No relationship between the measurable R-kaolin time and heparin concentration could be demonstrated (p=0.80), as well as no relationship between measurable TEG® Delta-kh R- time difference and heparin activity (p=0.42). However, we did identify a high probability to be able to predict a measurable R-kaolin time (negative predictive value 90%, 95% CI 74% to 98%) when heparin concentration is less than 1.24IU/ml. Conclusions: We were unable to predict heparin concentration using TEG® in this study. It is likely that this was related to methodological problems. The protamine dose was a complex calculation and there is uncertainty with regard to the actual amounts used. There were also multiple laboratory technicians, with a possible loss of standardization. However, R-kaolin time will likely be measurable at heparin concentrations below 1.24 IU/ml, and not measurable above that value. This observation is immensely valuable for clinicians and researchers. Future studies should take this into account and attempt to determine the relationship between TEG® Delta-kh R- time differences and heparin activity only when heparin concentration are less than 1.24IU/ml.
- ItemLactate concentration and oxygen flux post cardiopulmonary bypass: a pilot study(2020-06) Schoeman, Doreen; Smit, Marli; Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Anesthesiology and Critical Care.ENGLISH ABSTRACT: Objective: To identify the incidence and the main contributing factor of postoperative hyperlactataemia following cardiopulmonary bypass surgery. Design: Single-centre, prospective, non-randomized, observational pilot study. Setting: Tertiary hospital, University setting. Participants: Twenty-six patients who all underwent cardiopulmonary bypass for elective cardiac surgery and who met the inclusion criteria. We excluded patients with pre-existing conditions or medications that could possibly alter lactate metabolism or contribute to aerobic increase in lactate production. Interventions: Observational. Measurements: Arterial lactate, mixed venous oxygen saturations (SvO2), haemoglobin, arterial saturation, and mixed venous partial pressure (PvO2) were measured. Delivery of oxygen (DO2) and oxygen consumption (V𝑂𝑂̇2) were calculated for the first twelve postoperative hours. Factors potentially influencing V𝑂𝑂̇ 2 (temperature, shivering, pain, anxiety, the use of inotropic support, and the presence or absence of ventilation) were also documented. Main results: Transient hyperlactataemia (that peaked between postoperative hours two to eight) occurred in 47% of cases following cardiopulmonary bypass. Postoperative hyperlactataemia occurred as a result of an increase in oxygen consumption (V𝑂𝑂̇ 2). The use of adrenaline and an increase in temperature (as a result of passive rewarming) were identified as the contributing factors responsible for this V 𝑂𝑂̇ 2 increase. Postoperative delivery of oxygen (DO2) remained adequate; as illustrated by normal to high cardiac output, haematocrit, and arterial saturations.