Comparison of pulsed Doppler and thermodilution methods for measuring cardiac output in critically ill patients

We obtained 145 consecutive cardiac output measurements in 38 critically ill patients, using the invasive thermodilution and the noninvasive pulsed Doppler methods. The mean thermodilution cardiac output (TDCO) was 5.7 +/- 1.87 L/min and the mean pulsed Doppler cardiac output (PDCO) was 5.16 +/- 1.66 L/min. The mean difference between the two measurements was 0.51 L/min with an SD greater than 1.6 L/min, reflecting the scattering of results. The overall correlation coefficient was .58. The intercepts were large and the regression equation some way from the line of equal values (TDCO = 2.28 + 0.66 PDCO). When the results were analyzed according to diagnosis or by group experience, there were some differences in the bias of the estimate; however, the SD of the difference between methods was greater than one liter/min in all groups. Thus, the pulsed Doppler method failed to estimate accurately TDCO in critically ill patients.     

Correction of cardiac output obtained by Modelflow from finger pulse pressure profiles with a respiratory method in humans

The beat-by-beat non-invasive assessment of cardiac output (Q litre x min(-1)) based on the arterial pulse pressure analysis called Modelflow can be a very useful tool for quantifying the cardiovascular adjustments occurring in exercising humans. Q was measured in nine young subjects at rest and during steady-state cycling exercise performed at 50, 100, 150 and 200 W by using Modelflow applied to the Portapres non-invasive pulse wave (Q(Modelflow)) and by means of the open-circuit acetylene uptake (Q(C2H2)). Q values were correlated linearly ( r = 0.784), but Bland-Altman analysis revealed that mean Q(Modelflow) - Q(C2H2) difference (bias) was equal to 1.83 litre x min(-1) with an S.D. (precision) of 4.11 litre x min(-1), and 95% limits of agreement were relatively large, i.e. from -6.23 to +9.89 litre x min(-1). Q(Modelflow) values were then multiplied by individual calibrating factors obtained by dividing Q(C2H2) by Q(Modelflow) for each subject measured at 150 W to obtain corrected Q(Modelflow) (Qcorrected) values. Qcorrected values were compared with the corresponding Q(C2H2) values, with values at 150 W ignored. Data were correlated linearly ( r = 0.931) and were not significantly different. The bias and precision were found to be 0.24 litre x min(-1) and 3.48 litre x min(-1) respectively, and 95% limits of agreement ranged from -6.58 to +7.05 litre x min(-1). In conclusion, after correction by an independent method, Modelflow was found to be a reliable and accurate procedure for measuring Q in humans at rest and exercise, and it can be proposed for routine purposes.     

Mathematical coupling does not explain the relationship between right ventricular end-diastolic volume and cardiac output

OBJECTIVE: To evaluate the clinical significance of mathematical coupling on the correlation between cardiac output and right ventricular end-diastolic volume (RVEDV) through measurement of cardiac output by two independent techniques. DESIGN: Prospective, observational study. SETTING: Surgical intensive care unit in a level 1 trauma center. PATIENTS: Twenty-eight critically ill surgical patients who received mechanical ventilation and hemodynamic monitoring with a pulmonary artery catheter. INTERVENTIONS: A pulmonary artery catheter designed to measure right ventricular ejection fraction (RVEF) and cardiac output by the intermittent bolus thermodilution (TDCO) method and continuous cardiac output by the pulsed thermal energy technique was placed. A computerized data logger was used to collect data simultaneously from the RVEF/TDCO system and the continuous cardiac output system. MEASUREMENTS AND MAIN RESULTS: Two hundred forty-nine data sets from 28 patients were compared. There is statistical correlation between TDCO and continuous cardiac output measurements (r = 0.95, p < 0.0001) with an acceptable bias (-0.11 L/min) and precision (+/-0.74 L/min). The correlation was maintained over a wide range of cardiac outputs (2.3-17.8 L/min). There is a high degree of correlation between RVEDV and both TDCO (r = 0.72, p < 0.0001) and independently measured continuous cardiac output (r = 0.68, p < 0.0001). These correlation coefficients are not statistically different (p = 0.15). CONCLUSIONS: The continuous cardiac output technique accurately approximates cardiac output measured by the TDCO method. RVEDV calculated from TDCO correlates well with both TDCO and independently measured continuous cardiac output. Because random measurement errors of the two techniques differ, mathematical coupling alone does not explain the correlation between RVEDV estimates of preload and cardiac output.     

Lower body positive pressure by anti-G garment inflation: a suitable method to increase pulmonary capillary wedge pressure in healthy elderly subjects

In a study on non-invasive assessment of pulmonary capillary wedge pressure (PCWP), we sought a method to increase PCWP non-invasively. We hypothesized that inflation of an anti-G garment was suitable to increase PCWP non-invasively in healthy elderly subjects. In 20 subjects, aged 70 +/- 4 years (mean +/- SD), before, immediately after, and 4 min after anti-G garment inflation to 52 mmHg, PCWP and mean pulmonary artery pressure (MPAP) were measured with a Swan-Ganz catheter, and mean arterial blood pressure (MAP) with Finapres, in supine and semi-recumbent position. Supine, PCWP (mmHg, mean +/- SD) increased from 9.9 +/- 2.1 to 15.5 +/- 3.9** immediately after inflation and 13.4 +/- 3.7** at 4 min; semi-recumbent from 8.9 +/- 2.0 to 17.5 +/- 3.3** and 14.7 +/- 2.9** (*P<0.05, **P< 0.001 versus before inflation). MPAP (mmHg) increased after inflation: supine 16.9 +/- 2.3 to 22.3 +/- 4.6** and 20.6 +/- 3.9** and semi-recumbent 15.7 +/- 2.8 to 24.3 +/- 5.1** and 22.5 +/- 3.5**, suggesting that increased preload was the primary effect of anti-G garment inflation. Supine MAP (mmHg) increased from 96.0 +/- 11.3 to 101.4 +/- 13.4** and 100.5 +/- 12.7* and semi-recumbent from 102.0 +/- 8.9 to 108.3 +/- 11.4** and 106.0 +/- 11.3*, suggesting an effect of increased afterload as well. The latter was supported by an increase in total peripheral resistance (d s cm(-5)) from 1346 +/- 299 to 1441 +/- 384 after 4 min (P = 0.057) and from 1461 +/- 341 to 1532 +/- 406 (P = 0.054), supine and semi-recumbent respectively, while cardiac output remained unchanged. Complications did not occur. We conclude that in healthy elderly subjects, anti-G garment inflation is a safe, non-invasive, method to induce a significant increase in PCWP. Our findings justify its application in future studies in which non-invasive temporary increase in PCWP is required.     

Non-invasive cardiac output assessment during moderate exercise: pulse contour compared with CO2 rebreathing

The arterial pulse contour method called Modelflow 2·1 calculates stroke volume continuously, beat to beat, from the non-invasive blood pressure signal measured by Finapres or Portapres. Portapres is the portable version of Finapres. The purpose of this study was to compare cardiac output (CO) calculated using Modelflow 2·1 (CO_mf) with CO obtained by the CO₂ rebreathing method (CO_re) during steady state at moderate exercise levels. Twelve subjects visited the laboratory twice and performed submaximal exercise on a bicycle ergometer at 20%, 40% and 60% of their individual peak power output (PO_peak). The averaged correlation between CO_mf and CO_re gives an r-value of 0·69, whereas the slope and intercept of the regression line were 1·06 and 1·65 respectively. The averaged difference between CO_mf and CO_re was 2·27 ± 3·9 l min^–1 (mean ± standard deviation). However, the test–retest difference between CO_mf and CO_re was 2·5 ± 3·1 and 0·5 ± 1·3 l min^–1 respectively. These results suggest that Modelflow 2·1 is not an accurate method for estimating CO from non-invasive blood pressure data collected by Portapres during exercise at up to 60% of the individual PO_peak corresponding with daily life activity.     

Non-invasive ultrasonic cardiac output measurement in intensive care unit

A non-invasive method for measuring cardiac output utilizing M-mode echography and pulsed Doppler ultrasound is described. Measurements were obtained in 26 of 29 randomly selected, mechanically ventilated patients. These values were compared with simultaneously measured cardiac outputs by thermodilution. There was a statistically significant linear relationship between Cardiac Output measured by Doppler (DCO) and Thermodilution (TDCO): DCO = 0.86 TDCO + 0.29 1/min (r = 0.96, N = 26, SEE = 0.45 1/min) over the range of 1.75-8.5 1/ min. DCO had the additional advantage of measuring peak flow velocity and maximal blood flow acceleration during early systole, indices of left ventricular pumping ability. Ultrasonic monitoring of cardiac output may be an important supplement to invasive methods in critical care.     

Cardiac output by Modelflow method from intra-arterial and fingertip pulse pressure profiles

Modelflow, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q, litre x min(-1)). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q with Modelflow, so we compared Modelflow beat-by-beat Q values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0 +/- 2.9 years; weight, 81.2 +/- 12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly ( P < 0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q obtained from the finger (Qporta) was significantly ( P < 0.05) higher than that computed from the intra-arterial recordings (Qpia). The line relating beat-by-beat Qporta and Qpia was y =1.55 x -3.02 ( r2 = 0.640). The bias was 1.44 litre x min(-1) and the precision was 2.84 litre x min(-1). The slope of this line was significantly higher than 1, implying a systematic overestimate of Q by Qporta with respect to Qpia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q with an independent method.     

Continuous stroke volume monitoring by modelling flow from non-invasive measurement of arterial pressure in humans under orthostatic stress.

The relationship between aortic flow and pressure is described by a three-element model of the arterial input impedance, including continuous correction for variations in the diameter and the compliance of the aorta (Modelflow). We computed the aortic flow from arterial pressure by this model, and evaluated whether, under orthostatic stress, flow may be derived from both an invasive and a non-invasive determination of arterial pressure. In 10 young adults, Modelflow stroke volume (MFSV) was computed from both intra-brachial arterial pressure (IAP) and non-invasive finger pressure (FINAP) measurements. For comparison, a computer-controlled series of four thermodilution estimates (thermodilution-determined stroke volume; TDSV) were averaged for the following positions: supine, standing, head-down tilt at 20 degrees (HDT20) and head-up tilt at 30 degrees and 70 degrees (HUT30 and HUT70 respectively). Data from one subject were discarded due to malfunctioning thermodilution injections. A total of 155 recordings from 160 series were available for comparison. The supine TDSV of 113+/-13 ml (mean+/-S.D.) dropped by 40% to 68+/-14 ml during standing, by 24% to 86+/-12 ml during HUT30, and by 51% to 55+/-15 ml during HUT70. During HDT20, TDSV was 114+/-13 ml. MFSV for IAP underestimated TDSV during HDT20 (-6+/-6 ml; P<0.05), but that for FINAP did not (-4+/-7 ml; not significant). For HUT70 and standing, MFSV for IAP overestimated TDSV by 11+/-10 ml (HUT70; P<0.01) and 12+/-9 ml (standing; P<0.01). However, the offset of MFSV for FINAP was not significant for either HUT70 (3+/-8 ml) or standing (3+/-9 ml). In conclusion, due to orthostasis, changes in the aortic transmural pressure may lead to an offset in MFSV from IAP. However, Modelflow correctly calculated aortic flow from non-invasively determined finger pressure during orthostasis.     

Cardiac resynchronization therapy optimization by ultrasonic cardiac output monitoring (USCOM) device

OBJECTIVES: We investigated the accuracy and feasibility of a 2D echo-independent ultrasonic continuous wave Doppler cardiac output monitoring device (USCOM) operated by trained nurse for the atrio-ventricular interval (AVI) optimization in cardiac resynchronization therapy (CRT). BACKGROUND: CRT is of proven benefit in patients with advanced chronic heart failure and ventricular conduction delay. Appropriate AVI selection is critical to optimize hemodynamic in CRT. Currently, most non-invasive methods for AVI optimization are often complicated and labor-intensive. Methods: USCOM method, Ritter method, and aortic outflow cardiac output method were used to determine the optima AVI in 20 patients with CRT. The accuracy and time for measurement of each method were determined. RESULTS: The optimal AVI determined by USCOM method had good correlation with Ritter's method and aortic outflow estimated cardiac output method (r2= 0.78, P < 0.01 and r2= 0.73, P < 0.01, respectively). The optimal AVI determined USCOM method showed good agreement (within 10 msec range) with Ritter's method (85% patients) and aortic outflow estimated cardiac output method (80%). The mean time for determining AVI using USCOM method was shorter than that with aortic outflow method (7.1 +/- 0.7 min vs 12.7 +/- 1.1 min, P < 0.01), whereas the mean time was shortest for Ritter method (4.7 +/- 1.6 min vs 7.1 +/- 0.7 min, P < 0.01). CONCLUSION: USCOM device operated by trained nurse can provide a simple, accurate, and fast non-invasive method for the AVI optimization in CRT population.     

Lithium dilution cardiac output measurement: a clinical assessment of central venous and peripheral venous indicator injection

OBJECTIVE: The lithium indicator dilution technique has been shown to measure cardiac output (CO) accurately by using central venous injection of lithium chloride (Li-CCO). This study aimed to compare the measurement of CO by using peripheral venous administration of lithium chloride (Li-PCO) with Li-CCO. DESIGN: Prospective, observational human study. SETTING: Surgical intensive care unit. PATIENTS: Thirty-one patients were studied after major surgery. All patients had arterial, central, and peripheral venous catheters. A total of 24 patients had pulmonary artery catheters. MEASUREMENTS: Serial measurements of Li-CCO and Li-PCO were made during hemodynamically stable conditions. CO was also measured using thermodilution (TDCO) when a pulmonary artery catheter was present. Data were analyzed by linear regression, the generalized estimating equation, and the comparison method described by Bland and Altman. MAIN RESULTS: There were 93 Li-CCOs, 93 Li-PCOs, and 216 TDCOs recorded. The ranges of COs were similar: Li-CCO, 2.36-11.52 L/min (mean, 5.22 L/min; n = 31); Li-PCO, 1.63-9.99 L/min (mean, 5.22 L/min; n = 31), and TDCO, 3.28-10.4 L/min (mean, 5.75 L/min; n = 24). There was good linear correlation between Li-CCO and Li-PCO (R2 =.845). The mean difference for Li-CCO-Li-PCO was very small and insignificant (p =.97), and the limits of agreement were acceptable (mean difference +/- sd, 0.0005 +/- 0.64 L/min). The mean difference for Li-CCO-Li-PCO was smaller if the peripheral injection site was proximal rather than distal to the wrist (p =.053). Li-PCO and Li-CCO values were lower than simultaneously obtained TDCO measurements (Li-PCO-TDCO, -0.538 +/- 0.95 L/min, p =.003; Li-CCO-TDCO, -0.526 +/- 0.67 L/min, p =.0001). CONCLUSIONS: Li-PCO gives a measurement that agrees well with Li-CCO. Accuracy of Li-PCO is probably improved if a proximal arm vein is used. Li-PCO provides accurate measurements of CO without the risks of pulmonary artery or central venous catheterization.     

Disparities in circulatory adjustment to standing between young and elderly subjects explained by pulse contour analysis.

1. The circulatory adjustment to standing was investigated in two age groups. Young subjects consisted of 20 healthy 10-14-year-old girls and boys. Elderly subjects consisted of 40 70-86-year-old healthy and active females and males. Continuous responses of blood pressure and heart rate were recorded by Finapres. A pulse contour algorithm applied to the finger arterial pressure waveform was used to assess stroke volume responses. 2. During the first 30s (initial phase), an almost identical drop in mean blood pressure was found in both age groups (young, 16 +/- 10 mmHg; old, 17 +/- 10 mmHg), but the initial heart rate increase was attenuated in the elderly subjects (young, 29 +/- 7 beats/min; old, 17 +/- 7 beats/min). 3. During the period from 30 s to 10 min of standing, mean blood pressure increased from 96 +/- 12 to 106 +/- 12 mmHg in the elderly subjects compared with almost no change in the young subjects (from 82 +/- 8 to 84 +/- 7 mmHg). In the elderly subjects a progressive increase in total peripheral resistance (from 114 +/- 14% to 146 +/- 29%) was found, compared with an initial rapid increase in total peripheral resistance (126 +/- 18% after 30 s) with no further change during prolonged standing (124 +/- 17% after 10 min) in the young subjects. In this age group the decrease in stroke volume and the increase in heart rate after 10 min of standing were large (young, -37 +/- 11% and 27 +/- 11 beats/min; old, -31 +/- 9% and 7 +/- 6 beats/min, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Continuous noninvasive cardiac output determination using the CNAP system: evaluation of a cardiac output algorithm for the analysis of volume clamp method-derived pulse contour

The CNAP system (CNSystems Medizintechnik AG, Graz, Austria) provides noninvasive continuous arterial pressure measurements by using the volume clamp method. Recently, an algorithm for the determination of cardiac output by pulse contour analysis of the arterial waveform recorded with the CNAP system became available. We evaluated the agreement of the continuous noninvasive cardiac output (CNCO) measurements by CNAP in comparison with cardiac output measurements invasively obtained using transpulmonary thermodilution (TDCO). In this proof-of-concept analysis we studied 38 intensive care unit patients from a previously set up database containing CNAP-derived arterial pressure data and TDCO values obtained with the PiCCO system (Pulsion Medical Systems SE, Feldkirchen, Germany). We applied the new CNCO algorithm retrospectively to the arterial pressure waveforms recorded with CNAP and compared CNCO with the corresponding TDCO values (criterion standard). Analyses were performed separately for (1) CNCO calibrated to the first TDCO (CNCO-cal) and (2) CNCO autocalibrated to biometric patient data (CNCO-auto). We did not perform an analysis of trending capabilities because the patients were hemodynamically stable. The median age and APACHE II score of the 22 male and 16 female patients was 63 years and 18 points, respectively. 18 % were mechanically ventilated and in 29 % vasopressors were administered. Mean ± standard deviation for CNCO-cal, CNCO-auto, and TDCO was 8.1 ± 2.7, 6.4 ± 1.9, and 7.8 ± 2.4 L/min, respectively. For CNCO-cal versus TDCO, Bland–Altman analysis demonstrated a mean difference of +0.2 L/min (standard deviation 1.0 L/min; 95 % limits of agreement ?1.7 to +2.2 L/min, percentage error 25 %). For CNCO-auto versus TDCO, the mean difference was ?1.4 L/min (standard deviation 1.8 L/min; 95 % limits of agreement ?4.9 to +2.1 L/min, percentage error 45 %). This pilot analysis shows that CNCO determination is feasible in critically ill patients. A percentage error of 25 % indicates acceptable agreement between CNCO-cal and TDCO. The mean difference, the standard deviation, and the percentage error between CNCO-auto and TDCO were higher than between CNCO-cal and TDCO. A hyperdynamic cardiocirculatory state in a substantial number of patients and the hemodynamic stability making trending analysis impossible are main limitations of our study.     

Randomized controlled trial of home-based exercise training to evaluate cardiac functional gains.

There is evidence that multiple benefits can be obtained through exercise training that leads to increases in peak oxygen consumption (V(O(2))). It is unclear whether significant improvements can also be achieved through unsupervised low-budget home-based training regimes, especially in terms of cardiac functional gains. A randomized cross-over trial was conducted to investigate the effects of a home-based unsupervised exercise training programme of moderate intensity on aerobic capacity, cardiac reserve and peak cardiac power output in healthy middle-aged volunteers. Nine subjects with no known cardiovascular diseases performed symptom-limited treadmill cardiopulmonary exercise tests after an 8-week period of exercise training, and results were compared with those obtained after a similar 'non-exercising' control period. Cardiac output was measured non-invasively during exercise tests using the CO(2)-rebreathing method. With exercise training, resting heart rate decreased significantly from 88.3+/-3.4 to 78.7+/-3.2 beats.min(-1) (P<0.05), heart rate at a submaximal workload (V(O(2))=1.5 litres.min(-1)) decreased from 125.5+/-2.4 to 115.5+/-1.6 beats.min(-1), and peak V(O(2)) increased by 9% from 2.62+/-0.19 to 2.85+/-0.18 litres.min(-1) (P<0.01). Baseline cardiac power output was 1.11+/-0.05 W, and this remained unchanged with training. Peak cardiac power output increased by 16% from 4.1+/-0.3 to 4.7+/-0.3 W (P<0.001), and cardiac reserve increased by 21% (P<0.01). A major contribution to these increases was from the 11% increase in stroke volume, from 100.1+/-5.3 to 111.2+/-6.2 ml (P<0.001). All subjects reported more positive perceptions of their health (P<0.05), fitness (P<0.01) and levels of activity (P<0.01) after the training period. These results show that motivated subjects undergoing low-budget unsupervised home-based exercise training of moderate intensity can derive benefit in terms of symptoms, aerobic capacity and cardiac functional reserve.     

A modified single breath method for estimation of cardiac output in humans at rest and during exercise

This study was undertaken to determine the accuracy of a modification of a single breath method for estimation of cardiac output. The technique incorporated a single rebreathing stage followed by a prolonged expiration. Cardiac output was determined from the O2 uptake and the instantaneous changes in O2 and CO2 in the expired gas during the prolonged expiration. The mean values and the random errors (determined from the differences between pairs of estimates) of cardiac outputs in normal subjects at rest and exercise were 5.42 and +/- 0.60 litres/min (2 SD, 60 pairs) and 14.1 and +/- 1.8 litres/min (40 pairs). Larger random errors were obtained in a group of cardiac patients but, except in hypoxic patients, the mean values obtained by the single breath and the direct (Fick) methods were almost identical. We conclude that our modification of the single breath method is simple to use and sufficiently reliable for use in humans both at rest and during steady states of light exercise.     

Cardiac vagal response to water ingestion in normal human subjects

In healthy young subjects there is direct evidence for sympathetic vasoconstrictor activation after drinking water, but this is not accompanied by an increase in arterial blood pressure. A marked pressor response to water ingestion has, however, been observed in elderly subjects and in patients with autonomic failure. We examined the effect of water ingestion on haemodynamic variables and heart rate variability (HRV) markers of cardiac vagal control in ten healthy young subjects and four cardiac transplant recipients with confirmed persistent cardiac vagal denervation. In a random order crossover protocol, changes in heart rate, blood pressure and measures of high frequency (HF) HRV were compared over time following the ingestion of 500 ml and 20 ml (control) of tap water. In healthy subjects, after drinking 500 ml of water the heart rate fell from 67.6+/-2.0 (mean+/-S.E.M.) to 60.7+/-2.4 beats/min (P<0.01), and the bradycardic response peaked between 20 and 25 min. There were no significant changes in arterial blood pressure. Over the same time course, water ingestion caused increases in measurements of HF HRV: root-mean-square of successive RR interval differences (RMSSD) increased by 13+/-2.7 ms after 500 ml versus 2+/-3.1 ms after 20 ml (P<0.05); HF power increased by 686+/-400 versus -63+/-322 (P<0.01). In transplant recipients water ingestion was followed by a pressor response (range 13 to 29 mmHg). These results provide evidence that water ingestion in normal subjects is followed by an increase in cardiac vagal control that may counteract the pressor effects of sympathetic activation. We suggest that in the elderly, in transplant recipients and in autonomic failure, loss of this buffering mechanism explains the pressor response to drinking water.     

Evaluation of a noninvasive method for cardiac output measurement in critical care patients

OBJECTIVE: Thermodilution (TD) is the gold standard to monitor cardiac output (CO) in critical care. However, there is concern about the safety of right-ventricular catheterization. The CO(2) rebreathing technique allows noninvasive CO determination by means of the indirect Fick principle. Our objectives were: (a) to assess the accuracy of a new system of CO measurement using the CO(2) partial rebreathing method (PRCO); (b) to evaluate whether the PRCO itself may induce changes in CO. DESIGN AND SETTING: Prospective study in the intensive care department in a university-affiliated hospital. PATIENTS: Twenty-two mechanically ventilated critically ill patients. INTERVENTIONS: CO measured simultaneously by PRCO and TDCO. MEASUREMENTS AND RESULTS: PRCO and TDCO values were compared by concordance analysis. Stability of cardiac output during PRCO was evaluated by comparing the TDCO measurements before, during, and after the partial rebreathing period using analysis of variance. From a total of 79 valid sets of measurements, bias and precision was calculated at -0.18+/-1.39 l/min. The concordance analysis of lower and intermediate CO values (<7 l/min) yielded a bias and precision calculation of -0.07+/-0.91 l/min. No changes in hemodynamics were observed during the partial rebreathing period. CONCLUSIONS: The noninvasive partial CO(2) rebreathing technique may be an alternative method for CO determination in mechanically ventilated critically ill patients. The rebreathing maneuver alone does not induce changes in CO.     

Cardiac output by Portapres

Portapres derives continuous estimates of cardiac output from the peripheral pulse and has the potential to be an extremely valuable physiological and clinical tool. We assessed Portapres estimates of cardiac output in healthy subjects at rest, during maximal treadmill exercise ( n = 8) and during decreases caused by orthostatic stress ( n = 8). Comparison with a rebreathing method indicated that Portapres tended to overestimate cardiac output. The random errors of the estimates (precision), expressed as +/- 2 S.D. of the differences between paired estimates during steady states, ranged between 1.2 and 2.6 litres/min. We conclude that these errors indicate that the method is probably only useful for assessing changes in individual subjects where large changes are anticipated, as during exercise. When smaller changes occur, as during orthostasis, the errors preclude the use of individual subject data and only permit group average data to be examined.     

Ageing impairs insulin-mediated vasodilatation but not forearm glucose uptake

BACKGROUND: It is unclear if insulin-mediated vasodilatation is altered by ageing and if this affects insulin-mediated glucose uptake. MATERIAL AND METHODS: A 2-h euglycaemic hyperinsulinaemic clamp (56 mU m(-2) min(-1)) was performed in 10 healthy, nonobese elderly men (70-75 years) and 13 young men (23-28 years). Forearm blood flow (FBF) was measured by venous occlusion plethysmography and forearm glucose uptake was calculated by arterial and venous serum glucose determinations in the forearm. RESULTS: Insulin induced an increase in FBF in the younger men (from 3.9 +/- 1.1 SD to 5.9 +/- 2.2 mL min(-1) 100(-1)mL tissue, P < 0.001), but this insulin-mediated vasodilatation was completely blunted in the elderly subjects. Glucose extraction during the clamp was significantly higher in the elderly subjects (1.2 +/- 0.76 vs. 0.82 +/- 0.37 mmol L(-1) at 120 min, P < 0.01), resulting in a similar forearm glucose uptake in the two groups. On the other hand, whole-body glucose uptake was significantly decreased in the elderly subjects (5.3 +/- 1.8 vs. 8.0 +/- 1.1 mg kg(-1) min(-1), P < 0.001). CONCLUSION: The present study showed that the ability of insulin to induce vasodilatation is blunted in the forearm in healthy, nonobese elderly subjects. However, the elderly compensate for this impairment with an increased glucose extraction from arterial blood to maintain an unaltered forearm glucose uptake.     

Influence of indomethacin on the systemic and pulmonary vascular resistance in man.

1. Indomethacin, an inhibitor of the cyclo-oxygenase system that converts arachidonic acid into prostaglandins and related substances, was infused intravenously in 12 healthy volunteer subjects. 2. Systemic systolic and diastolic blood pressures and heart rate were recorded in all subjects, and in most of them also the systemic arteriovenous oxygen difference, the total oxygen uptake and the pulmonary arterial and wedge pressures. 3. The infusion of indomethacin was followed by a decreased cardiac output (from 7.3 +/- 0.3 to 6.3 +/- 0.3 litres/min) and an increased mean systemic blood pressure (from 92 +/- 1 to 102 +/- 1 mmHg), indicating an elevation of the total systemic vascular resistance (from 98 +/- 4 to 124 +/- 5 kPa 1(-1) s) by indomethacin. The ventilation and the pulmonary vascular resistance did not change after the infusion of indomethacin. 4. The results suggest that products formed by the cyclo-oxygenase system at rest exert a relaxing effect in certain parts of the systemic vascular bed, thereby lowering the systemic vascular resistance.     

Effect of an inspiratory impedance threshold device on hemodynamics during conventional manual cardiopulmonary resuscitation

BACKGROUND: In animals in cardiac arrest, an inspiratory impedance threshold device (ITD) has been shown to improve hemodynamics and neurologically intact survival. The objective of this study was to determine whether an ITD would improve blood pressure (BP) in patients receiving CPR for out-of-hospital cardiac arrest. METHODS: This prospective, randomized, double-blind, intention-to-treat study was conducted in the Milwaukee, WI, emergency medical services (EMS) system. EMS personnel used an active (functional) or sham (non-functional) ITD on a tracheal tube on adults in cardiac arrest of presumed cardiac etiology. Care between groups was similar except for ITD type. Low dose epinephrine (1mg) was used per American Heart Association Guidelines. Femoral arterial BP (mmHg) was measured invasively during CPR. RESULTS: Mean+/-S.D. time from ITD placement to first invasive BP recording was approximately 14 min. Twelve patients were treated with a sham ITD versus 10 patients with an active ITD. Systolic BPs (mean+/-S.D.) [number of patients treated at given time point] at T = 0 (time of first arterial BP measurement), and T=2, 5 and 7 min were 85+/-29 [10], 85+/-23 [10], 85+/-16 [9] and 69+/-22 [8] in the group receiving an active ITD compared with 43+/-15 [12], 47+/-16 [12], 47+/-20 [9], and 52+/-23 [9] in subjects treated with a sham ITD, respectively (p < 0.01 for all times). Diastolic BPs at T = 0, 2, 5 and 7 min were 20+/-12, 21+/-13, 23+/-15 and 25+/-14 in the group receiving an active ITD compared with 15+/-9, 17+/-8, 17+/-9 and 19+/-8 in subjects treated with a sham ITD, respectively (p = NS for all times). No significant adverse device events were reported. CONCLUSIONS: Use of the active ITD was found to increase systolic pressures safely and significantly in patients in cardiac arrest compared with sham controls.