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PubMed1994

Effects of red cell transfusion on cardiac output and blood flow velocities in cerebral and gastrointestinal arteries in premature infants.

Anaemia may increase the risk of tissue hypoxia in preterm infants. The effect of transfusion on circulation was studied in 33 preterm infants with a mean (SD) gestational age of 29 (5) weeks (range 26-34), birth weight 1153 (390) g (range 520-1840), and postnatal age of 48 (21) days (range 19-100). Packed cell volume, blood viscosity (capillary viscometer), cardiac output, and cerebral blood flow velocities in the internal carotid artery, anterior cerebral artery, and coeliac trunk (Doppler ultrasound) were determined before and after transfusion of 10 ml/kg of packed red blood cells. Transfusion increased packed cell volume from a mean (SD) 0.27 (0.45) to 0.37 (0.48). Mean arterial blood pressure did not change while heart rate decreased significantly from 161 (14) l/min to 149 (12). Cardiac output decreased from 367 (93) ml/kg/min to 311 (74) due to decrease in stroke volume from 2.28 (0.57) ml/kg to 2.14 (0.46) and in heart rate. There was a significant increase in systemic red cell transport (cardiac output times packed cell volume) by 17%, systemic flow resistance (blood pressure to cardiac output ratio) by 23%, and blood viscosity by 33%. Vascular hindrance (flow resistance to blood viscosity ratio) did not change significantly, thereby suggesting that neither vasoconstriction nor vasodilation occurred with transfusion. After transfusion blood flow velocities decreased significantly in the anterior cerebral artery by 23%, in the internal carotid artery by 8%, and in the coeliac trunk by 12%. Red cell transport estimated as products of blood flow velocities times packed cell volume increased significantly by 25% in the internal carotid artery and by 21% in the coeliac trunk. These results indicate that red cell transfusion improved systemic oxygen transport as well as oxygen transport in the internal carotid artery and coeliac trunk.

Blood Flow Velocity↗
PubMed1997

Bioimpedance cardiac output measurements in patients with presumed congestive heart failure.

OBJECTIVE: To describe preliminary ED experience with thoracic electrical bioimpedance (TEB) for evaluation of patients with complaints suggestive of congestive heart failure (CHF). METHODS: A 6-month, prospective, observational study was performed using a convenience sample of patients with signs and symptoms consistent with CHF. Patients were excluded if they had received medication prior to arrival in the ED, if they were obese, and if they had unstable vital signs. They also were excluded if they were combative, refused to sign consent, or had invasive lines that did not allow for TEB lead placement. Patients also were excluded if the study could not be completed because the patient was taken from the department for a diagnostic test, or if there were no good follow-up records available 6-12 months after the patient's visit. The patient's physician was blinded to the output of the TEB monitor. Cardiac output (CO), stroke volume (SV), end-diastolic volume (EDV), thoracic fluid index (TFI), and acceleration index (ACI) were recorded at 5-minute intervals. Results were evaluated for the time intervals 0-5 minutes, 30-35 minutes, and 60-65 minutes. RESULTS: Seven patients were included in the study. The echocardiographic diagnoses were hypertrophic cardiomyopathy (2 cases), dilated cardiomyopathy (2 cases), ischemic cardiomyopathy (1 case), right ventricular hypertrophy (1 case), and pericardial effusion (1 case). Significant changes were seen in all cardiac parameters, with variance from individual to individual. CONCLUSIONS: Significant differences in TEB variables exist between patients who appear similar on initial examination in the ED. Changes noted on TEB may help to further elucidate physiologic differences. The clinical use of TEB-based hemodynamic measurements to guide presumed CHF patient management remains speculative.

Cardiac Output↗
PubMed1990

Hemodynamic status susceptible to slowing of heart rate during thermodilution cardiac output determination in anesthetized patients.

To identify hemodynamic variables that might indicate susceptibility to slowing of heart rate (HR) and to mean arterial pressure (MAP) decrease caused by cold injectate during thermodilution (TD) cardiac output determination, we measured hemodynamic variables in 32 anesthetized patients undergoing major surgery. A total of 608 cardiac output determinations were evaluated for any relationship between the magnitude of HR decreases and basal hemodynamic variables. The magnitude of HR decrease was pronounced in low cardiac index (CI), low mean pulmonary artery pressure (MPAP), and high systemic vascular resistance index (SVRI). Although there was some decrease in MAP associated with cold injectate, neither changes in SVRI nor those in the other hemodynamic variables correlated with the decreases in MAP. These results suggest that decreased CI and MPAP associated with elevated SVRI may be more susceptible to slowing of HR during cardiac output determination by TD in anesthetized patients.

Adult↗
PubMed1988

Optimization of oxygen transport in mechanically ventilated newborns using oximetry and pulsed Doppler-derived cardiac output.

In respiratory distress syndrome (RDS), PEEP improves arterial oxygenation but may impair cardiac output. The effects of PEEP on gas exchange and hemodynamics were studied in 12 mechanically ventilated newborns in the acute phase of RDS. Stepwise increase in PEEP resulted in both a) a progressive increase in PaO2 and transcutaneous oxyhemoglobin saturation, and b) a depression of pulsed Doppler-measured cardiac output that was statistically significant at 9 cm H2O PEEP. Thus, averaged systemic oxygen delivery (DO2) was maintained with improved arterial oxygenation up to 6 cm H2O PEEP. Further increase in PEEP induced a significant fall in DO2. No variation was observed in heart rate and mean arterial pressure. The combined use of oximetry and pulsed Doppler echocardiography enables noninvasive optimization of mechanical ventilation and PEEP during the clinical course.

Acute Disease↗
PubMed1991

AANA Journal course: new technologies in anesthesia: update for nurse anesthetists--noninvasive, continuous, cardiac output monitoring by thoracic electrical bioimpedance. 16.

Risk management and cost containment concerns inherent in central venous cannulation and pulmonary artery catheter insertion have prompted the search for noninvasive cardiac output methods. Thoracic electrical bioimpedance is one such method, revitalized since the early days of space flight. Thoracic electrical bioimpedance measures the impedance changes associated with plethysmographic changes within the thoracic cavity and determines cardiac output. An appreciation of the foundational principles underlying thoracic electrical bioimpedance when compared to the Fick, indicator dilution and Doppler cardiac output monitoring methods will facilitate the nurse anesthetist's understanding and utilization of these modalities.

Cardiac Output↗
PubMed2006

[Determining cardiac output by carbon dioxide rebreathing in patients with sleep apnea-hypopnea syndrome].

The objective of the present study was to determine the relation between resting cardiac output in patients with sleep apnea-hypopnea syndrome but without arterial hypertension or heart failure as measured indirectly by the carbon dioxide rebreathing method and left ventricular function evaluated by transthoracic echocardiography. We also compared the variability and reproducibility of the measurements obtained by the equilibrium and exponential methods. In patients with sleep apnea-hypopnea syndrome there was a modest but significant association between resting cardiac output and left ventricular shortening fraction (r=0.690; P<.001) and left ventricular ejection fraction (r=0.690; P<.001). In addition, mean (SD) cardiac output obtained by the equilibrium method showed a lower coefficient of variability (0.21 [0.08]) than that of the exponential method (0.16 [0.09]) (P<.01) as well as a narrower reproducibility interval.

Carbon Dioxide↗
PubMed2003

Decreased 2,3-diphosphoglycerate concentration in low cardiac output patients and its influence on the determination of in vivo p50.

We investigated whether 2,3-diphosphoglycerate (2,3-DPG) is altered in patients with low cardiac output and the influence of its concentration on the calculation of in vivo P(50). Biochemical and blood gas analysis were performed along with the measurement of cardiac output and body temperature in 13 patients submitted to cardiopulmonary bypass surgeries without the use of donor blood. In vivo P(50) was calculated using the measured (P(50m)) and the estimated 2,3-DPG (P(50e)). 2,3-DPG concentration was lower in these patients when compared to the values obtained in normal volunteers (6.9 +/- 2.2 vs. 11.9 +/- 2.4 microm/gHb). P(50m) was lower than P(50e) (21.6 +/- 1.1 vs. 30.1 +/- 1.2 mm Hg) at all time points. Our data show that in patients with low cardiac output, 2,3-DPG concentration is reduced. Therefore, in these patients, the use of standard values for this variable may introduce an error in the calculation of in vivo P(50).

2,3-Diphosphoglycerate↗
PubMed1993

Vasodepressor neurons in medulla alter cardiac contractility and cardiac output.

We injected neuroexcitatory and neuroinhibitory agents into the depressor region of the caudal ventrolateral medulla of anesthetized rabbits and determined the effect on arterial pressure, myocardial contractility, cardiac output, and plasma catecholamines and neuropeptide Y. Brief excitation of the sympathoinhibitory neurons with medullary injection of L-glutamate reduced arterial pressure, peripheral vascular resistance, and myocardial contractility. Cardiac output was unaffected. Prolonged inhibition of the sympathoinhibitory neurons with medullary injection of muscimol increased arterial pressure, peripheral vascular resistance, and myocardial contractility. There was a progressive fall in cardiac output. These changes were accompanied by an increase in plasma neuropeptide Y and plasma norepinephrine, but no change in plasma epinephrine. Our findings indicate that the sympathoinhibitory vasomotor neurons in the caudal ventrolateral medulla tonically suppress the activity of sympathetic preganglionic neurons controlling myocardial contractility as well as peripheral vasomotor tone. Dysfunction of these medullary neurons could underly some forms of experimental hypertension.

Animals↗
PubMed1992

Beat-by-beat analysis of cardiac output and blood pressure responses to short-term barostimulation in different body positions.

Rapid quantification of the human baro-reflex control of heart rate has been achieved on a beat-by-beat basis using a neck-chamber with quick ECG-triggered pressure changes. Referring to recent findings on heart rate and stroke volume, the present study uses this technique to compare cardiac output as well as blood pressure changes in supine and upright position to investigate feedback effects and to confirm postural reflex modifications not revealed by RR-interval changes. A suction profile starting at +40 mmHg and running 7 steps of pressure decrease down to -65 mmHg was examined in 0 degree and 90 degrees tilting position while beat-by-beat recordings were done of heart rate, stroke volume (impedance-cardiography) and blood pressure (Finapres (tm)) (n=16). The percentual heart rate decrease failed to be significantly different between positions. A suction-induced stroke volume increase led to a cardiac output almost maintained when supine and significantly increased when upright. A decrease in all blood pressure values was found during suction, except for systolic values in upright position which increased. Conclusively, (a) it is confirmed that different inotropy accounts for the seen gravitational effect on the cardiac output not represented by heart rate (b) identical suction levels in different positions lead to different stimuli at the carotid receptor. This interference has to be considered in microgravity studies by beat-by-beat measurement of cardiac output and blood pressure.

Adult↗
PubMed1991

The effect of haematocrit on transthoracic electrical impedance and on the calculation of cardiac output by an impedance cardiograph.

The Transthoracic electrical impedance (TEI) was measured using the Bomed NCCOM3 non-invasive cardiac output monitor in 27 patients with polycythemia rubra vera (PCRV) and in a control group of 27 patients with normal haematocrits. The mean haematocrit was 49.4% (SD 2.61) in the patients with PCRV and 42.1% (SD 2.95) in the control group, a difference that was significant (p less than 0.001). The mean TEI was also significantly higher in patients with PCRV than in the control group (p less than 0.05), the respective values being 31.25 (5.48) Ohms and 27.5 (3.31) Ohms. The mean values for cardiac output (CO) and cardiac index (CI) were similar in both groups.

Cardiac Output↗
PubMed2000

Simultaneous comparison of thoracic bioimpedance and arterial pulse waveform-derived cardiac output with thermodilution measurement.

OBJECTIVE: To compare the accuracy and reliability of thoracic electrical bioimpedance (TEB) and the arterial pulse waveform analysis with simultaneous measurement of thermodilution cardiac output (TD-CO) in critically ill patients. DESIGN: Prospective data collection. SETTING: Emergency department and critical care unit in a 2,000-bed inner-city hospital. PATIENTS: A total of 29 critically ill patients requiring invasive hemodynamic monitoring for clinical management were prospectively studied. INTERVENTIONS: Noninvasive cardiac output was simultaneously measured by a TEB device and by analysis of the arterial pulse waveform derived from the finger artery. Invasive cardiac output was determined by the thermodilution technique. MEASUREMENTS AND MAIN RESULTS: A total of 175 corresponding TD-CO and noninvasive hemodynamic measurements were collected in 30-min intervals. They revealed an overall bias of 0.34 L/min/m2 (95% confidence interval, 0.24-0.44 L/min/m2; p < .001) for the arterial pulse waveform analysis and of 0.61 L/min/m2 (95% confidence interval, 0.50-0.72 L/min/m2; p < .001) for the TEB. In 39.4% (n = 69) of all measurements, the discrepancy between arterial pulse waveform analysis and TD-CO was >0.50 L/min/m2. The discrepancies of the arterial pulse waveform analysis correlated positively with the magnitude of the cardiac index (r2 = 0.29; p < .001). In 56.6% (n = 99) of all measurements, the discrepancy between TEB and TD-CO was >0.50 L/min/m2. The magnitude of the discrepancies of the TEB was significantly correlated with age (r2 = 0.17; p = .02). Measurements were in phase in 93.2% of all arterial pulse waveform analysis and in 84.9% of all TEB readings (p < .001). CONCLUSIONS: The arterial pulse waveform analysis exhibits a greater accuracy and reliability as compared with the TEB with regard to overall bias, number of inaccurate readings, and phase lags. The arterial pulse waveform analysis may be useful for the monitoring of hemodynamic changes. However, both methods fail to be a substitute for the TD-CO because of a substantial percentage of inaccurate readings.

Adult↗
PubMed2003

A differentiable, periodic function for pulsatile cardiac output based on heart rate and stroke volume.

Many mathematical models of human hemodynamics, particularly those which describe pressure and flow pulses throughout the circulatory system, require as specified input a modeling function which describes cardiac output in terms of volume per unit time. To be realistic, this cardiac output function should capture, to the greatest extent possible, all relevant features observed in measured physical data. For model analysis purposes, it is also highly desirable to have a model function that is continuous, differentiable, and periodic. This paper addresses both classes of needs by developing such a function. Physically, the present function provides an accurate model for flow into the ascending aorta. It is completely specified by a minimal number of standard input parameters associated with left ventricle dynamics, including heart rate, mean cardiac output, and an estimation of the peak-to-mean flow ratio. Analytically, it can be expressed as a product of two continuous, differentiable and periodic factors. Further, the Fourier expansion of this model function is shown to be a finite Fourier series, and explicit closed-form expressions are given for the non-zero coefficients in this series.

Animals↗
PubMed1988

Direct Fick cardiac output: are assumed values of oxygen consumption acceptable?

The use of assumed values of oxygen consumption has become an accepted practice in the calculation of direct Fick cardiac output. A survey showed that the assumed values in common use were derived from basal metabolic rate studies on normal subjects, a use which may not be valid. We have compared previous assumed values based on basal metabolic rate or cardiac catheterization studies with those obtained by direct measurement in 80 patients (age range 38-78 years) with various cardiac disorders. Comparison of the assumed and directly measured values of indexed oxygen consumption and the cardiac index showed large discrepancies, with over half the values differing by more than +/- 10% and many by more than +/- 25% from the measured value. Assumed values of oxygen consumption should be used with caution when calculating cardiac output during cardiac catheterization procedures, because large errors can result. The equations of LaFarge and Miettinen gave the closest approximation to the measured data and their use is recommended in preference to values predicted from basal metabolic rate studies.

Adult↗
PubMed1991

Cardiac output, oxygen consumption and arteriovenous oxygen difference following a sudden rise in exercise level in humans.

1. To investigate the relative contributions of increases in cardiac output and arteriovenous oxygen difference to the increase in oxygen consumption during exercise, the ventilatory and cardiovascular responses to a sudden transition from unloaded cycling to 70 or 80 W were measured in six normal healthy subjects. 2. Oxygen consumption (VO2) was measured breath-by-breath and corrected for changes in lung gas stores. Cardiac output (Q) was measured beat-by-beat using pulsed Doppler ultrasound, and blood pressure was measured beat-by-beat using a non-invasive finger cuff (Finapres). All data were calculated off-line, second-by-second. 3. Arteriovenous oxygen difference (A-VO2) was calculated from Q and VO2 using the Fick Principle. Left ventricular afterload was calculated by dividing Q by mean blood pressure. 4. The data for Q and VO2 were closely fitted by single exponential curves (mean r2 0.84 and 0.90 respectively; r is the correlation coefficient). These curves yielded mean time constants for the increases in Q and VO2 of 28 and 55 s respectively following the increase in exercise level. In each individual subject, the time course of adjustment of Q was faster than that of VO2. There was a mean lag of 15 s from the start of the new exercise level before the derived A-V O2 began to increase; the mean time constant for A-V O2 was 57 s. 5. If A-V O2 had remained constant, the observed rise in Q alone would have resulted in an average of 87% of the increase in VO2 which was observed after 5 s. If Q had remained constant, the observed increase in A-V O2 would have led to only 8% of the actual increase in VO2 after 5 s. 6. Mean and systolic blood pressure rose and afterload fell immediately after the onset of the increased workload. The time constants of the systolic blood pressure and afterload responses to exercise varied widely and ranged from 37 to 81 and 10 to 26 s respectively (n = 4). 7. We conclude that Q is responsible for most of the early increase in VO2 following a sudden increase in exercise workload. Blood pressure responses to exercise are slower than Q and VO2 responses, probably due to the rapid decrease in afterload. 8. The dominant contribution of Q to adaptation to changing workload may be physiologically important particularly in heart disease, where decreased ability to increase cardiac output may limit the capacity to cope with changing metabolic needs during everyday activities.

Adaptation, Physiological↗
PubMed1995

Do changes in cardiac output affect the inspiratory to end-trial oxygen difference?

BACKGROUND: The paramagnetic technique has made it possible to monitor the end-tidal oxygen concentration and P(1-ET)O2, i.e. inspiratory to end-tidal oxygen difference, breath-by-breath. Little is known about the implications of a changing P(1-ET)O2, but so far studies have shown it to be a quick and sensitive variable to detect hypoventilation. This study was designed to observe the circulatory effects on P(1-ET)O2 in an experimental setting but monitored as in a clinical situation. METHODS: We assessed the oxygen difference during changes in cardiac output induced by intravenous ephedrine-hydrochloride in 12 healthy male volunteers. P(1-ET)O2 was measured with a fast-response paramagnetic differential oxygen sensor. Cardiac output was measured with non-invasive transthoracic electrical bioimpedance. As simultaneous changes in metabolism and ventilation will also influence P(1-ET)O2 oxygen uptake and expired minute volume were monitored. After a rest period, the subjects had an intravenous injection of ephedrine-hydrochloride 0.1 mg.kg-1 followed by a 30-min observation period. RESULTS: Cardiac output increased significantly as did the oxygen uptake and the ventilation. We found no biological significant correlation between cardiac output and P(1-ET)O2. The P(1-ET)O2 was influenced by ventilation and metabolism.

Adult↗
PubMed1996

Reproducibility of thermodilution cardiac output determination in critically ill patients: comparison between bolus and continuous method.

OBJECTIVE: A semi-continuous thermodilution method (CCO) was recently developed to measure cardiac output with less risk of bacterial contamination, fluid overload, and user-induced errors than the classical bolus technique (BCO). Previous comparison between these two methods showed negligible bias. However, large limits of agreement suggest that the two methods are not interchangeable. We hypothesized that this poor agreement may be due to differences in reproducibility. METHODS: In 23 critically ill patients, 369 paired measurements of CCO and BCO were compared (range of cardiac outputs: 2.8 to 16 L/min). The reproducibility of BCO and CCO methods was evaluated on a sample of 205 and 209 determinations, respectively. RESULTS: The comparison between the CCO and the BCO methods confirmed previous results: i.e., small bias (-0.39 L/min) and large limits of agreement (-2.06 to +1.28 L/min). Reproducibility showed no bias for either the CCO or the BCO method. Limits of reproducibility agreement between repeated determinations were approximately 50% less for CCO than for BCO method: respectively -0.87 to +0.82 L/min for the CCO method and -1.56 to +1.37 L/min for the BCO method. Consequently, the threshold necessary to ascertain that the difference between two measurements was not due to the internal variability of the method (3 x SEM) was 0.39 for the CCO method and 0.75 L/min for the BCO method. CONCLUSION: Differences in reproducibility may explain the poor agreement between the CCO and BCO methods. The better reproducibility of the CCO method allows the detection of smaller variations in cardiac output and suggests the superiority of this new method.

Cardiac Output↗
PubMedDate not supplied

The relationship between cardiac output and access flow during hemodialysis.

Satisfactory hemodialysis access flow (Qa) is necessary for dialysis adequacy. However, high access flows are postulated to increase cardiac output (CO). The relationship between Qa and CO is not well defined. The purpose of this study was to observe the relationship between Qa and CO and to evaluate the effect of blood volume change (BVdelta) on Qa and CO during hemodialysis (HD). Measurements of Qa and CO (ultrasound dilution; Transonics Monitor, Ithaca, NY) were performed sequentially at baseline in 18 patients (13 forearm arteriovenous fistulae, 5 Gore-Tex grafts) and after an intervention involving either HD with attempted zero BVdelta (mean: -0.4%; range: -2.6 to 1.6%) or a significant BVdelta (mean: -7.3%; range: -3.1 to -11.9%). Measurement of BVdelta was done by hematocrit dilution (Crit-Line Monitor, In-Line Diagnostics, Riverdale, UT). The volume ultrafiltered (V(UF)) and the mean arterial pressure (MAP) were recorded at baseline and after intervention. In five patients with fistulae, CO was measured after manual occlusion of the fistula for 1 min. At baseline, mean (+/-SD) Qa was 1455+/-600 ml/min, and CO was 6.8+/-1.8 L/min. The relationship between Qa and CO was strong, Qa = 0.20 CO + 0.06 (r = 0.62; p = 0.01); this was not significantly altered with either intervention. Access flow was not changed with either zero BVdelta or significant BVdelta. Cardiac output was not altered when there was no BVdelta; however, CO did decrease by 1.2+/-0.6 L/min (p<0.001) after BVdelta reduction. The Qa/CO ratio was unchanged after zero BVdelta but was increased after BVdelta (p = 0.004). There were no correlations with MAP change or V(UF). There were no differences in Qa, CO, or Qa/CO by access type. The mean Qa/CO was 21+/-6%. Three patients had Qa/CO <15%, and they all had access stenoses. Cardiac output did not decrease after transient (1 min) occlusion of the fistula. In conclusion, there is a strong relationship between Qa and CO. With BVdelta, the Qa is maintained while the CO falls and the Qa/CO increases, perhaps by reflex vasoconstriction of the systemic circulation. Longitudinal studies are required to determine which is the dependent variable. A low Qa/CO may indicate access dysfunction.

Arteriovenous Anastomosis↗
PubMed1994

Bactericidal antibiotics increase tumor necrosis factor-alpha and cardiac output in rats after cecal ligation and puncture.

We hypothesized that treatment of experimental sepsis with bactericidal antibiotics, known to enhance microbial toxin release, would alter tumor necrosis factor-alpha production and the hemodynamic response to the syndrome. In the rat, after cecal ligation and puncture (CLP), elevated serum TNF levels and cardiac output were observed following antibiotic treatment. TNF and cardiac output were elevated to a greater extent in bactericidal-treated than bacteriostatic-treated or antibiotic-untreated rats. Animals treated with bactericidal antibiotics also had significantly greater cardiac outputs than untreated rats. Despite increases in circulating TNF with antibiotic administration, the mortality rate at 96 hr decreased after either bactericidal or bacteriostatic antibiotics. We conclude that elevated TNF after CLP in rats treated with antibiotics is associated with enhanced hemodynamic responses to CLP, but does not increase early mortality. In this model of polymicrobial sepsis, bactericidal and bacteriostatic antibiotics led to different hemodynamic effects without compromising survival.

Ampicillin↗