Comparison of continuous non-invasive finger arterial pressure monitoring with conventional intermittent automated arm arterial pressure measurement in patients under general anaesthesia.

BACKGROUND: For a majority of patients undergoing anaesthesia for general surgery, mean arterial pressure (MAP) is only measured intermittently by arm cuff oscillometry (MAPiNIAP). In contrast, the Nexfin(®) device provides continuous non-invasive measurement of MAP (MAPcNIAP) using a finger cuff. We explored the agreement of MAPcNIAP and MAPiNIAP with the gold standard: continuous invasive MAP measurement by placement of a radial artery catheter (MAPinvasive). METHODS: In a total of 120 patients undergoing elective general surgery and clinically requiring MAPinvasive measurement, MAPiNIAP and MAPcNIAP were measured in a 30 min time period at an arbitrary moment during surgery with stable haemodynamics. MAPiNIAP was measured every 5 min. RESULTS: Data from 112 patients were analysed. Compared with MAPinvasive, modified Bland-Altman analysis revealed a bias (sd) of 2 (9) mm Hg for MAPcNIAP and -2 (12) mm Hg for MAPiNIAP. Percentage errors for MAPcNIAP and MAPiNIAP were 22% and 32%, respectively. CONCLUSIONS: In a haemodynamically stable phase in patients undergoing general anaesthesia, the agreement with invasive MAP of continuous non-invasive measurement using a finger cuff was not inferior to the agreement of intermittent arm cuff oscillometry. Continuous measurements using a finger cuff can interchangeably be used as an alternative for intermittent arm cuff oscillometry in haemodynamically stable patients, with the advantage of beat-to-beat haemodynamic monitoring. CLINICAL TRIAL REGISTRATION: NCT 01362335 (clinicaltrials.gov).

Implications of automated creatine kinase (CK)-MM1,2,3/CK-MB1,2 isoform analysis as an early marker for the detection of myocardial tissue damage.

Measurement of creatine kinase (CK) isoforms enables the clinician to detect myocardial tissue damage at an early stage after myocardial infarction. According to the manufacturer's specifications, it should be possible to perform CK isoform analysis automatically using the new Cardio Rep analyser. In order to investigate the suitability of this new analyser we measured the CK MM1-3, and CK MB1 and 2 isoform patterns, firstly in 30 patients with acute myocardial infarction (AMI), for whom total CK and CK-MB levels were ordered, and secondly in 23 patients with chest pain suspected as having AMI (n = 11) or with unstable angina pectoris (UAP) (n = 12). The total time for analysis, including 5 min pre- and 10 min post-analyser run time, was found to be 40 min. For elevated MB2/MB1 ratios there is a discrepancy between the MB2/MB1 ratios determined from the densitometric scans concerning the surface and the peak height ratios. The MB2/MB1 ratios of the studied AMI patients exceeded the upper reference limits approximately 2 h after the onset of symptoms, whereas the CK-MB and total CK levels increased after about 6 h. The MB2/MB1 ratios from the patients with UAP were either below the detection limit or these patients could be discriminated from patients with AMI when low CK-MB and total CK levels were considered in conjunction. From our results we conclude that assessment of CK isoforms can be performed relatively simply with the new analyser within 40 min. However, for reliable calculation of the MB2/MB1 ratios, the curve monitoring of the MB2-MB1 densitometric scans should be improved. The CK isoforms are useful as an early marker for AMI as their reference interval is already exceeded approximately 2 h after an AMI. Moreover, CK isoform analysis might prove to be useful in discriminating at an early stage between AMI and other causes of chest pain. This could decrease the number of patients with a false-positive diagnosis admitted to coronary care units, resulting in a reduction of costs.