Predictors Of Cardiac Output Research Articles

Estimation of Total Cardiac Output Using Non-Invasive Parameters in HeartMate 3 Patients

<h3>Purpose</h3> In patients on left ventricle assist device (LVAD) support, total cardiac output (CO) results from the summation of LVAD flow and native flow through the aortic valve. Our study aims to: 1) quantify discrepancies between LVAD flow and total CO, and 2) test a novel approach to estimate total CO using non-invasive parameters in patients implanted with a HeartMate 3 (HM3), a centrifugal pump that features intrinsic pulse technology to prevent stasis within the pump. <h3>Methods</h3> Patients implanted with a HM3 between 11/2014 and 12/2017 were retrospectively studied. CO by thermodilution (TD) was measured in triplicate and the average was used for subsequent analyses. A total of 17 concurrently acquired variables were considered as potential predictors of CO: age, gender, weight, BMI, BSA, hemoglobin (Hb), hematocrit, LVEF, LVEDd, SBP, DBP, MAP, HR, LVAD flow, speed, PI and power. A multiple linear regression model was fit with the above predictor variables and CO by TD as the dependent variable to derive the <i>HM3 CO Formula</i>. To assess validity of the <i>HM3 CO Formula</i> against CO by TD, Pearson's correlation coefficients (r), mean absolute difference (MAD) and mean observed difference (MOD) were calculated<i>.</i> <h3>Results</h3> 69 HM3 patients (age 60±11y, 84% male, ischemic 43%, BMI 29±5.4 kg/m²) were studied. LVAD flow had good correlation but poor agreement with total CO by TD (r= 0.455, p<0.0001; MAD±SE 1.33±0.13 l/min, MOD±SE 1.15±0.15 l/min, <b>Fig A</b>). The <i>HM3 CO formula</i> incorporating SBP, Hb, LVAD Power, and weight (CO = 1.197 + 0.028 x SBP -0.372 x Hb + 0.734 x power + 0.021 x weight) had better correlation and agreement with CO by TD (r= 0.714, p <0 .0001; MAD±SE 0.79±0.09 l/min, MOD±SE -0.05 ± 0.13 l/min, <b>Fig B</b>). <h3>Conclusion</h3> In HM3 patients, LVAD flow does not provide good estimate of total CO. The <i>HM3 CO Formula</i> offers an alternative method to estimate total CO using non-invasive parameters. Validation studies are warranted to confirm these preliminary findings.

Right Atrial Pacing to Improve Acute Hemodynamics in Pulmonary Arterial Hypertension

Pacing to increase resting heart rate (HR) is commonly employed in order to improve hemodynamics and cardiac output (CO), particularly in post-operative setting when right ventricle (RV) dysfunction is present. We tested if right atrial (RA) pacing improves RV hemodynamics acutely, and if the degree of baseline RV dysfunction modifies this relationship. We prospectively enrolled adult subjects with known or suspected pulmonary arterial hypertension (PAH) who underwent elective right heart catheterization between January 2013 and April 2016. RV pressure-volume (PV) analysis was performed with conductance catheters. RV volumes were calibrated by cardiac MRI same day. After measuring baseline PV data, a bipolar pacing wire was positioned in the RA and rate set to 80 to 90 beats per minute (bpm). Rate was increased in steps of 20 bpm. PV loops were recorded at end-expiration after 1 minute in each group: 80-99, 100-119, and 120-139 bpm. Parametric data were analyzed by Repeated Measures ANOVA, and non-parametric data were analyzed by Friedman Test. Baseline hemodynamic predictors of CO were analyzed by Repeated Measures simple linear regression. Twenty-three subjects were included in this analysis. Baseline mean RA pressure was 7 ± 3 mmHg with pulmonary vascular resistance of 5.2 ± 4.1 wood units. As HR increased with RA pacing, stroke volume (SV) declined in each pacing group (68±22, 61±19, 54±21 mL, respectively; p<0.001) with increase in CO (5.5±1.9, 6.2±1.9, 6.6±2.5 L/min; p<0.001). The dP/dt maximum increased (429, 490, 549 mmHg/s; p<0.001); however, RV-pulmonary arterial coupling (Ees/Ea) fell with pacing (0.97 vs 0.84 vs 0.78, p=0.009). No baseline hemodynamic parameter or measure of RV function modified the relationship between CO and RA pacing. Between-subject data had large variation; exclusion of non-PAH subjects (n=6) did not alter results. As heart rate increases with RA pacing, RV contractility and CO increase modestly at the expense of cardiac efficiency.

Donor B-type natriuretic peptide predicts early cardiac performance after heart transplantation

Decision processes in heart donation remain difficult and are often based on subjective evaluation. We measured B-type natriuretic peptide (BNP) in heart donors and analyzed its value as a discriminator for early post-transplant cardiac performance. Blood samples were prospectively obtained in 94 brain-dead patients, among whom 56 were scheduled for heart donation. BNP values were not available prior to donor selection. BNP of heart donors was related to invasively measured cardiac output and hemodynamic parameters, early after transplantation. BNP, expressed as median (interquartile range), was 65 (32 to 149) pg/ml in brain-dead donors scheduled for heart donation. BNP was higher (287 pg/ml, range 65 to 457; p = 0.0001) in donors considered ineligible for heart donation. In 45 heart recipients, cardiac output (CO) of 5.6 (4.8 to 6.2) liters/min was measured at Day 12 (10-15). In the univariate analysis, recipient CO correlated significantly with donor BNP (r = -0.34, p = 0.025). Stepwise multiple regression, including donor variables such as body mass index, age, BNP, norepinephrine dose, gender and total ischemic time, identified donor BNP and age as the best independent predictors of CO in recipients (p = 0.02 and p = 0.005, respectively, R(2) of the model = 0.27). Donor BNP of >160 pg/ml had 89% accuracy to predict poor cardiac performance in the recipient (cardiac index <2.2 liters/min/m(2)). High donor BNP was independently correlated with a longer hospital stay. Donor BNP was found to be related to cardiac performance, early after cardiac transplantation. BNP measurement in heart donors could become a useful tool in the evaluation of donor hearts.

Sequential patterns of haemodynamic and metabolic changes in experimental hypovolaemic shock. II. Responses to reinfusion of shed blood.

The haemodynamic and metabolic effects which follow the infusion of blood in experimental hypovolaemia have not been studied in detail. The 10 dogs that survived 90 min of hypovolaemia in a study of bleeding (Pardy and Dudley, 1979) were investigated during and shortly after the reinfusion of shed blood using the same techniques. Data from 9 animals were suitable for analysis. As with bleeding, 6 sequential phases were identified; reinfusion of blood was completed in the fifth phase. Initial reinfusion was associated with a rapid improvement in haemodynamic and metabolic status, although mean arterial pH fell because carbon dioxide production increased. Maximum metabolically effective tissue perfusion was probably attained in phase II, but haemodynamic improvement continued until phase IV. Arterial pH did not rise above the pre-infusion value until phase V, and this rise was the result of a fall in PaCO2 secondary to a reduction in physiological dead space and an increase in buffering capacity. Pulmonary artery pressure was superior to systemic artery pressure as a predictor of cardiac output during blood volume restoration. A number of conclusions pertaining to clinical practice are drawn.

The transthoracic impedance cardiogram is a potential haemodynamic sensor for an automated external defibrillator.

The American Heart Association has endorsed the concept of Public Access Defibrillation. However, there have been reports of inappropriate direct current shocks from automatic external defibrillators. The specificity of automatic external defibrillators for shockable rhythms may be improved by the incorporation of a haemodynamic sensor. This study examined the use of four parameters extracted from the impedance cardiogram i.e. Peak dz/dt (the peak of the impedance cardiogram measured from the line dz/dt=0 ohms(-1)), Peak-trough (the peak-to-trough measurement of the impedance cardiogram ohms(-1)), Area 1 (the area under the C wave of the impedance cardiogram above the line dz/dt=0 mohm) and Area 2 (the area under the impedance cardiogram 50 ms on either side of the Peak and above the line dz/dt=0 mohm) as predictors of cardiac output. At 116 cardiac arrest calls the ECG and impedance cardiogram were recorded through two ECG/defibrillator pads placed in an antero-apical position. Nine recordings were rejected for artefact. The rhythm recorded in the remaining 107 calls was asystole (19), ventricular fibrillation (14), agonal rhythm (20), electromechanical dissociation (22), ventricular tachycardia (27) and sinus rhythm (5). These rhythms were divided into those associated with haemodynamic collapse i.e. no pulse -- asystole, ventricular fibrillation, agonal rhythm, electromechanical dissociation and shockable ventricular tachycardia (associated with loss of consciousness, pulselessness or a systolic blood pressure of <80 mmHg) (Group 1) and those associated with a satisfactory cardiac output i.e. non-shockable ventricular tachycardia (conscious with a pulse) and sinus rhythm (Group 2). On univariate analysis each of the four impedance cardiogram parameters were significantly greater in Group 2 than Group 1 (P<0.001). On multivariate analysis the parameters which best differentiated the two groups were Area 1 and Peak-trough. Thus the impedance cardiogram is a potential haemodynamic sensor for an automatic external defibrillator.

Noninvasive determination of cardiac output using single breath CO2 analysis.

To examine the utility of single breath CO2 analysis as a noninvasive measure of cardiac output. An animal laboratory in a university-affiliated medical center. A prospective, animal cohort study comparing 21 parameters derived from single breath CO2 analysis with cardiac output determined by an ultrasonic flow probe. Six healthy adult sheep. The single breath CO2 analysis station consists of a mainstream capnometer, a variable orifice pneumotachometer, a signal processor, and computer software with capability for both on- and off-line data analysis. Twenty-one derived components of the CO2 expirogram were evaluated as predictors of cardiac output. Cardiac output was manipulated by successive injections of a hydraulic constrictor placed around the inferior vena cava. Thirty-four measurements of cardiac output were available for comparison with derived variables from the CO2 expirogram. Stepwise linear regression identified two variables that were most predictive of cardiac output: a) the angle between the slope lines for phase II and III of the CO2 expirogram divided by the volume of CO2 per breath (angle/mL CO2); and b) the slope of phase II. The multivariate equation was highly statistically significant and explained 94% of the variance (adjusted r2 = .94, p < .0001). The bias and precision of the calculated cardiac output were .00 and .23, respectively. The mean percent difference for the cardiac output estimate derived from the single breath CO2 analysis station was 0.36%. Our data indicate that analysis of the CO2 expirogram can yield accurate information about the cardiovascular system. Specifically, two variables derived from a plot of expired CO2 concentration vs. expired volume predict changes in cardiac output in healthy adult sheep with an adjusted coefficient of determination of .94. Prospective application of this technology in the setting of lung injury and rapidly changing physiology will be essential in determining the clinical usefulness of the technique.

Mixed Venous Oxygen Saturation as a Predictor of Cardiac Output in the Postoperative Cardiac Surgical Patient

Mixed venous oxygen saturation (SvO 2) 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 SvO 2 and CI was 0.05 ± 0.42, and was not significantly different from zero. Although the mean correlation coefficient between the change in SvO 2 and the change in CI was significant ( p < .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 SvO 2 was not predictive of a CI less than 2 L/min/m 2, a level of cardiac performance that might require intervention. In conclusion, SvO 2 was not predictive of CI postoperatively in the cardiac surgical patient.