[Unconsciousness]. / Tajuttomuus.

Unconsciousness is a directly life-threatening condition that requires immediate action to reveal its cause. The cause of unconsciousness is usually metabolic or toxic and in the rest of the cases structural and intracranial. Unconsciousness results from a disturbance of function of either the reticular activating system or both cerebral hemispheres. Treatment of an unconscious person begins with the confirmation of vital functions. Special attention is paid on head and neck injuries, meningism, pupillary inequality and papillary stasis. Both radiological and laboratory investigations are usually required. Owing to its quickness, CT scan of the head is the basic neurological examination, adequately revealing the common intracranial causes. Treating an unconscious patient calls for the complete range of a physician's expertise. Determined action and knowledge of common and treatable diseases will, however, bring the situation under control.

Effects of levosimendan on renal function in patients undergoing coronary artery surgery.

OBJECTIVES: To evaluate the effect of levosimendan on postoperative renal function in patients with compromised heart function undergoing on-pump coronary artery bypass graft surgery. DESIGN: A prospective, randomized, placebo-controlled, double-blind substudy. SETTING: Cardiothoracic surgery, anesthesiology, and intensive care units at 2 university hospitals. PARTICIPANTS: Sixty patients with left ventricular ejection fraction ≤50% were randomized into 2 parallel treatment groups. INTERVENTIONS: Levosimendan or placebo was started after the induction of anesthesia with a 12-µg/kg bolus in 10 minutes followed by the infusion of 0.2 µg/kg/min for the next 23 hours and 50 minutes. MEASUREMENTS AND RESULTS: Serum cystatin C and plasma creatinine were measured at baseline; at 6 and 24 hours after declamping the aorta; and on the 1st, 2nd, and 5th postoperative days. Urine N-acetyl-ß-glucosaminidase (U-NAG) was measured at baseline and at 6 and 24 hours after declamping of the aorta. Renal function was estimated with calculated glomerular filtration rate (eGFR). The changes in plasma creatinine, serum cystatin C, and urine NAG were not significant among the placebo and the levosimendan groups at any of the measuring points. CONCLUSIONS: After coronary artery surgery, levosimendan did not have a significant influence on the kidney function measured with these specific kidney markers.

Increased preoperative thrombin generation and low protein S level associated with unfavorable postoperative hemodynamics after coronary artery bypass grafting.

In a previous study, preoperative levels of activated protein C (APC) were associated with unfavorable postoperative hemodynamics after coronary artery bypass grafting (CABG). Protein C is activated by thrombin. Protein S, the cofactor of activated protein C, has activated protein C-independent anticoagulant activity and cytoprotective effects. Therefore, the objective of this study was to test whether preoperative, baseline levels of either thrombin or protein S were associated with hemodynamic performance or markers of myocardial damage after CABG. One hundred patients undergoing elective on-pump CABG were prospectively studied. Prothrombin fragment F1+2 (a marker of thrombin generation) and free protein S were measured preoperatively and cardiac index, systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI) were measured serially thereafter at fixed time points. Cardiac biomarkers CK-MBm and TnT were measured postoperatively. There was an inverse correlation between preoperative F1+2 and free protein S levels (r= -0.30, p=0.003). High preoperative F1+2 and low preoperative protein S levels were associated with a less favorable hemodynamic profile postoperatively. Patients with F1+2 in the highest decile (≥0.85 nmol/l) and patients with preoperative protein S in the lowest decile (≤63%) had lower CI values, and higher pulmonary and systemic vascular resistance index values postoperatively than comparison patients. Preoperative F1+2 or protein S did not correlate with postoperative cardiac biomarker levels. Baseline activation of coagulation and the balance between pro-coagulant and anti-coagulant factors preoperatively might have implications for postoperative hemodynamic recovery after CABG.

Levosimendan in perioperative and critical care patients.

PURPOSE OF REVIEW: To present recent experiences and studies on the pharmacologic profile of levosimendan in the context of surgery, anesthesia and critical care. Special emphasis is on the studies that could support the use of or create novel indications for levosimendan in these patients. RECENT FINDINGS: Several controlled studies now suggest that levosimendan is efficacious in improving hemodynamics in patients after cardiac surgery. Its use as an adjunct to catecholamines instead of phosphodiesterase inhibitors can be recommended in patients with postcardiotomy heart failure and cardiogenic shock. Prophylactic administration before cardiopulmonary bypass in patients with compromised ventricular function may also be rational because levosimendan facilitates weaning from cardiopulmonary bypass without inotropes with higher myocardial oxygen cost of inotropy. This mode of administration also seems to attenuate troponin release and spares treatment resources such as duration of postoperative ventilation and ICU stay. The reported experience in patients with noncardiac surgery is meager but previous results obtained from nonsurgical patients should be largely applicable. The use of levosimendan in treating septic myocardial depression or sepsis syndrome is a promising option but remains investigational for today. SUMMARY: New practice advisories and proposals for indications to treat and prevent low-output syndrome in patients at risk are warranted for patients undergoing cardiac surgery with cardiopulmonary bypass. Levosimendan should also be considered as an adjunct drug for the treatment of cardiogenic shock. Further experience and controlled studies are needed to support the use of levosimendan for other perturbations in critical care and perioperative medicine.

Levosimendan facilitates weaning from cardiopulmonary bypass in patients undergoing coronary artery bypass grafting with impaired left ventricular function.

BACKGROUND: Levosimendan is a compound with vasodilatory and inotropic properties. Experimental data suggest effective reversal of stunning and cardioprotective properties. METHODS: This prospective, randomized, placebo-controlled, double-blind study included 60 patients with 3-vessel coronary disease and left ventricular ejection fraction (LVEF) of less than 0.50. Levosimendan administration (12 microg/kg bolus, followed by an infusion of 0.2 microg/kg/min) was started immediately after induction anesthesia. Predefined strict hemodynamic criteria were used to assess the success of weaning. If weaning was not successful, CPB was reinstituted and an epinephrine infusion was started. If the second weaning attempt failed, intraaortic balloon pumping (IABP) was instituted. RESULTS: The groups had comparable demographics. The mean (standard deviation) preoperative LVEF was 0.36 (0.8) in both groups. The baseline cardiac index was 1.8 (0.3) L/min/m(2) in the levosimendan group and 1.9 (0.4) L/min/m(2) in the placebo group. The mean duration of CPB to primary weaning attempt was 104 (25) minutes in the levosimendan and 109 (22) minutes in the placebo group. Primary weaning was successful in 22 patients (73%) in the levosimendan group and in 10 (33%) in the placebo group (p = 0.002). The odds ratio for failure in primary weaning was 0.182 (95% confidence interval, 0.060 to 0.552). Four patients in the placebo group failed the second weaning and underwent IABP compared with none in the levosimendan group (p = 0.112). CONCLUSIONS: Levosimendan significantly enhanced primary weaning from CPB compared with placebo in patients undergoing 3-vessel on-pump coronary artery bypass grafting. The need for additional inotropic or mechanical therapy was decreased.

Levosimendan reversing low output syndrome after heart transplantation.

After heart transplantation primary graft failure is a major cause of early mortality. Treatment options include inotropes and mechanical assist devices. Developing better methods would impact on patients' short- and long-term survival. We present a case of primary graft failure manifested as cardiogenic shock unresponsive to catecholamines and a phosphodiesterase inhibitor. Reversal of low output syndrome was achieved with a new type of inotropic agent, levosimendan, leading to the later complete recovery.