Continuous Fick cardiac output by fiberoptic oxymetry during aorto-coronary bypass surgery. A comparison with thermodilution cardiac output.
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Mixed venous oxygen saturation (SvO2) was measured continuously with a fiberoptic pulmonary artery catheter in 25 patients during the first 24 hours after cardiac surgery and was compared with the thermodilution cardiac index (CI). The mean correlation coefficient between SvO2 and CI was 0.05 +/- 0.42, and was not significantly different from zero. Although the mean correlation coefficient between the change in SvO2 and the change in CI was significant (p less than .05), the magnitude of the coefficient (0.19 +/- 0.44) indicates poor predictive value. The correlation did not improve when adjusted for multiple clinical variables, and the SvO2 was not predictive of a CI less than 2 L/min/m2, a level of cardiac performance that might require intervention. In conclusion, SvO2 was not predictive of CI postoperatively in the cardiac surgical patient.
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The authors examined the correlations between cerebral blood flow (CBF) during the stage of vasospasm following subarachnoid hemorrhage and four parameters, namely, cardiac output (cardiac index), mean arterial blood pressure, age, and the Glasgow coma scale score. Forty-two patients who were diagnosed to have subarachnoid hemorrhage were included in this study, and 50 measurements were performed between day 5 and 12 following the subarachnoid hemorrhage. The CBF was measured by stable xenon-enhanced CT and the mean values of four CBF maps were corrected for a PaCO2 of 34 mm Hg (CBF34). The cardiac output and cardiac index were continuously monitored during the CBF measurement. The correlation coefficients of cardiac index, mean arterial blood pressure, age, and GCS against CBF34 were, respectively, 0.436, 0.227, 0.037, and 0.225, and the p values were, respectively, 0.002, 0.074, 0.789, and 0.087. The CBF34 was positively correlated with only the cardiac index and not with any of the other three parameters. Therefore, an increase in the cardiac output is apparently associated with an increase in the CBF during the stage of vasospasm following subarachnoid hemorrhage. Furthermore, we measured the CBF and cerebral perfusion pressure before and after increasing cardiac output in three patients during the stage of vasospasm. The CBF increased by 22.5% +/- 2.9 (SD), with a 42.0% +/- 16.4 increase in the cardiac index, however, no significant change in cerebral perfusion pressure was observed. Therefore, the increase in CBF associated with the increase in cardiac output seems to be attributable to a reduction in the cerebrovascular resistance.
We describe a patient with severe left ventricular dysfunction simultaneously monitored with pulse contour cardiac output (PiCCO) analysis, a continuous cardiac output pulmonary artery catheter (continuous COPAC) and intraoperative transoesophageal echocardiography (TOE). There was good agreement between cardiac output (CO) measurements obtained by the three techniques prior to cardiopulmonary bypass (CPB). Agreement of CO measurements following CPB was initially pool; but improved following recalibration of PiCCO. PiCCO-derived global end-diastolic volume index (GEDVI) and cardiac function index (CFI), were assessed as markers of left ventricular preload and myocardial contractility, respectively. GEDVI correlated well with CO in the postoperative period. CFI increased more than two-fold following coronary revascularization and milrinone administration, and there was also a temporal relationship between the CFI and the dose of milrinone in the first 24 hours of treatment. Global end-diastolic volume and cardiac function index may be useful additional measures of left ventricular preload and myocardial contractility in patients with severe left ventricular dysfunction.
New mathematical algorithms have been applied to a computer controlled closed breathing circuit system for non-invasive measurement of cardiac output (COniv). This system has been described in an animal study. Forty patients were studied 5 and 18 hours after cardiac surgery using the thermodilution technique as the reference (COtd). The variables entered into the algorithms for COniv were oxygen uptake, carbon dioxide elimination, end-tidal carbon dioxide partial pressure, tidal volume and arterial oxygen saturation. Mixed venous carbon dioxide partial pressure was obtained from an automatically implemented short rebreathing manoeuvre. Pulmonary perfusion was calculated by a modified Fick equation for carbon dioxide and the shunt flow added to obtain COniv. During mechanical ventilation, there was a good agreement between COtd and COniv (r = 0.8). The bias was -0.14 l/min and the precision was 0.77 l/min. The reproducibility of COniv was 0.03 l/min and for COtd -0.03 l/min with a standard deviation of the difference being 0.35 l/min for COniv and 0.31 l/min for COtd. In awake, but sedated extubated patients, the method proved unsatisfactory on account for uneven tidal volumes and difficulties with leakage around the mouth piece. We conclude that this new technique provides reliable and reproducible measures of cardiac output in sedated, ventilated patients.
Measurement of volumetric cardiac output is technically difficult and poorly reproducible, and the technique is unsuitable for use in the majority of patients in whom a knowledge of overall cardiovascular function would be desirable. Interpretation of a single measurement in a patient is difficult because little is known about volumetric cardiac output in normal subjects and the available techniques of measurement are very complex or invasive. Linear cardiac output, in contrast, can be simply, non-invasively, and reproducibly measured at the bedside by doppler ultrasound. The systolic-velocity integral of a single heart beat (stroke distance) multiplied by the heart rate gives minute distance; this may be envisaged as the distance travelled by mid-stream blood in the aorta in a minute. Providing there is no aortic disease, minute distance may be used as an absolute indication of cardiac output and for following serial changes.
Cardiac output determined by Doppler echocardiography was compared with that determined by thermodilution at rest and during dobutamine infusion in 10 patients (group A) and by the Fick method at rest in 11 patients (group B). All patients had angina pectoris without valvular heart disease. Maximum spatial blood velocity and cross sectional aortic area were estimated by the Doppler technique and echocardiography. Cardiac output was calculated by multiplying blood velocity by aortic area at various levels in the ascending aorta. The best correlation of cardiac output between the invasive and non-invasive methods was obtained when maximum velocity in the aortic root and the aortic orifice area were used in the calculations. Cardiac output was considerably overestimated when area measurements in the aortic root were used.
Transoesophageal Doppler cardiac output measurement was evaluated against the thermodilution method in eleven patients undergoing elective cardiac surgery. A total of 106 pairs of Doppler and thermodilution values were obtained. Cardiac output was measured over a range of 2.3 l.min-1. to 11.51 l.min-1. The mean difference between the Doppler and thermodilution measures was -1.0 l.min-1 (thermodilution minus Doppler). Standard deviction was 1.8 l.min-1. This is a significant difference. It is concluded that these techniques do not agree when measuring cardiac outputs.
The relationship between cardiac output and the tissue distribution of alfentanil was investigated in seven healthy volunteers. Subjects were given 10 micrograms/kg alfentanil and 0.5 mg/kg indocyanine green. Arterial blood samples were obtained at baseline, 1 minute, every 1/2 minute until 5 minutes, and then every minute until 15 minutes after the drug injection was begun. Subsequent samples were collected to 6 hours. Cardiac output was measured continuously by use of thoracic bioimpedance. Alfentanil pharmacokinetics were modeled with both a standard three-compartment model and a four-compartmental model based in part on the two-compartmental pharmacokinetics of indocyanine green. The sum of intercompartmental clearances for both the three- and four-compartment models were significantly correlated with the measured cardiac outputs, r = 0.93 and r = 0.88, respectively. These findings indicate that the intercompartmental clearance (i.e., tissue distribution) of alfentanil is largely determined by cardiac output (i.e., tissue blood flow).
Previous investigators demonstrated divergent results, when comparing impedance to other established methods for the assessment of cardiac output. Cardiac output is defined as stroke volume multiplied by heart rate. Heart rate is easy to measure and the main determinant of cardiac output during exercise under physiologic conditions. Therefore, cardiac output (CO) by tetrapolar impedance cardiography (TIC) was compared to thermodilution (TD) in 35 patients (P). In a second step it was examined how heart rate alone would perform as a predictor of CO under exercise. Measurements were done at rest, 25, 50, 75, and 100 w. Results were corrected for hematocrit (HCT). There was no correlation between CO by TD and by TIC at rest (r = -0.006). Under exercise correlation was somewhat better with r = 0.45 despite correction for HCT. Mean values were similar, but scatter was wide. Relative increase in CO by both methods was also correlated (r = 0.46), while heart rate alone correlated best to TD (r = 0.65). Transthoracic impedance cardiography is not a reliable technique to measure absolute values of cardiac output at rest. During exercise large scatter limits this method to the measurement of CO in larger groups. At exercise heart rate alone appears to be a better indicator of increase of cardiac output than impedance cardiography.
OBJECTIVE: Commercially available semi-continuous cardiac output (SCCO) monitoring systems are based on the pulsed warm thermodilution technique. There is evidence that SCCO fails to correlate with standard intermittent bolus cardiac output (ICO) in clinical situations with thermal instability in the pulmonary artery. Furthermore, ventilation may potentially influence thermodilution measurements by enhanced respiratory variations in pulmonary artery blood temperature and by cyclic changes in venous return. Therefore, we evaluated the correlation, accuracy and precision of SCCO versus ICO measurements before and after extubation. DESIGN: Prospective cohort study. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS AND PARTICIPANTS: 22 cardiac surgical ICU patients. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: SCCO and ICO data were obtained at nine postoperative time points while the patients were on controlled mechanical ventilation. Further sets of measurements were taken during the weaning phase 20 min before extubation, and 5 min, 20 min and 1 h after extubation. SCCO and ICO measurements yielded 286 data pairs with a range of 1.8-9.9 l/min for SCCO and 1.9-9.8 l/min for ICO. The correlation between SCCO and ICO was highly significant (r = 0.92; p < 0.01), accompanied by a bias of -0.052 l/min and a precision of 0.56 l/min. Correlation, accuracy and precision were not influenced by the mode of respiration. CONCLUSIONS: Our results demonstrate excellent correlation, accuracy and precision between SCCO and ICO measurements in postoperative cardiac surgical ICU patients. We conclude that SCCO monitoring offers a reliable clinical method of cardiac output monitoring in ICU patients following cardiac surgery.
To determine whether renal prostaglandins participate in the regulation of renal blood flow during acute reduction of cardiac output, cardiac venous return was decreased in 17 anesthetized dogs by inflating a balloon placed in the thoracic inferior vena cava. This maneuver decreased cardiac output from 3.69+/-0.09 liters/min (mean+/-SEM) to 2.15+/-0.19 liters/min (P < 0.01) and the mean arterial blood pressure from 132+/-4 to 111+/-5 mm Hg (P < 0.01) and increased total peripheral vascular resistance from 37.6+/-2.5 to 57.9+/-4.8 arbitrary resistance units (RU) (P < 0.01). In marked contrast, only slight and insignificant decreases in the renal blood flow from 224+/-16 to 203+/-19 ml/min and renal vascular resistance from 0.66+/-0.06 to 0.61+/-0.05 arbitrary resistance units (ru) were observed during inflation of the balloon. Concomitant with these hemodynamic changes, plasma renin activity and plasma norepinephrine concentration increased significantly in both the arterial and renal venous bloods. Plasma concentration of prostaglandin E(2) in renal venous blood increased from 34+/-6 to 129+/-24 pg/ml (P < 0.01). The subsequent administration of indomethacin or meclofenamate had no significant effect on mean arterial pressure, cardiac output, and total peripheral vascular resistance, but reduced renal blood flow from 203+/-19 to 156+/-21 ml/min (P < 0.01) and increased renal vascular resistance from 0.61+/-0.05 to 1.05+/-0.21 ru (P < 0.01). Simultaneously, the plasma concentration of prostaglandin E(2) in renal venous blood fell from 129+/-24 to 19+/-3 pg/ml (P < 0.01). Administration of indomethacin to five dogs without prior obstruction of the inferior vena cava had no effect upon renal blood flow or renal vascular resistance. The results indicate that acute reduction of cardiac output enhances renal renin secretion and the activity of the renal adrenergic nerves as well as renal prostaglandin synthesis without significantly changing renal blood flow or renal vascular resistance. Inhibition of prostaglandin synthesis during acute reduction of cardiac output results in an increased renal vascular resistance and reduced renal blood flow. Accordingly, that data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during acute reduction of cardiac output.
The aim of this study was to test the accuracy of cardiac output assessment by Doppler and electromagnetic flowmetry in dogs during states of (1) marked enhancement in cardiac output, which was obtained by means of either isoprenaline infusion or treadmill exercise, or (2) reduction in cardiac output obtained by administration of phenylephrine. Additionally, in vitro comparisons were undertaken between Doppler and electromagnetic flow-probes and assessment of flow by direct volumetric measurement. These in vitro experiments showed a good correlation between timed volume collections and electromagnetic flow assessment up to high flow velocities. Doppler flow measurements underestimated the flow at high velocities. In both the resting dog and after phenylephrine, that is, at states with low heart rate and cardiac output, the waveforms of electromagnetic flow and Doppler velocity were similar for both phasic and mean flow, respectively. During states of cardiac stimulation Doppler flow showed a decrease in maximum velocity in the ascending aorta. Due to this decrease in peak flow velocity, mean Doppler blood flow did not increase despite of increased heart rate. This result cannot be explained on the basis of the deviation of Doppler measurements at high velocities in the in vitro experiments. Although our results are in contradiction with earlier studies, electromagnetic assessment seems to be more reliable in blood flow measurements in the ascending aorta. Hence, Doppler flow measurements should not be used uncritically for such quantitative flow assessment in large vessels as determination of cardiac output.
Heart rate, stroke volume, cardiac output and mean arterial blood pressure were followed from the resting pre-meal situation and for 2 hours after intake of standardized meals in four healthy individuals. Continuous records of stroke volume and cardiac output were achieved with an improved method of Doppler ultrasonography. A smallish meal and one 2 1/2 times larger were both given twice and in random order to each of the four test persons. The consumption of a meal invariably resulted in a cardiac output increase, which developed gradually to reach a maximum level 30 to 60 min after end of the meal. The postprandial cardiac output increase resulted from significant increases in both heart rate and stroke volume. There were distinct and significant differences between the circulatory responses to small and large meals. The increase in cardiac output after a large meal was considerably larger and lasted for longer than the increase after a small meal. Two hours after a small meal cardiac output was nearly or fully back to pre-meal values, while cardiac output was still markedly elevated 2 hours after a large meal. Consequently, the total 'extra' amount of blood delivered by the heart over 2 post-meal hours was significantly--about 100%--larger after the large meal than after the small one. Mean arterial blood pressure either fell or remained almost unchanged in the hour after a meal, so that total peripheral resistance was consistently and significantly reduced in the postprandial period--and considerably more so after a large meal than after a small one.
Cardiac output was measured in 11 patients during extra-corporeal detoxification after open heart surgery. All patients were mechanically ventilated and had pulmonary artery catheters for cardiac output (COT) measured by thermodilution. A sensor on the arterial side of the extracorporeal circulation measured flow and sound velocity transients. Injections of 2-5 ml 0.9% saline at 37 degrees C into the arterial line upstream of the sensor permitted its calibration; 10-20 ml of the same solution was injected intravenously or into the venous dialysis injection port, and cardiac output (COUD) was calculated by the ultrasound velocity dilution technique. COT was measured within 5 min of the ultrasound dilution measurement. CO was in the range of 2-8 L/m. The regression equation was COUD = 1.09 x COT-0.32 (r = 0.97, n = 31). These data suggest agreement between the ultrasound dilution technique and thermodilution. Ultrasound dilution is preferable in patients undergoing extracorporeal detoxification when pulmonary artery catheterization is not required or dangerous.