Cardiac power (PWR) is the continuous product of flow and pressure in the proximal aorta. Our aim was to validate the PWR integral as a marker of left ventricular energy transfer to the aorta, by comparing it to stroke work (SW) under multiple different loading and contractility conditions in subjects without obstructions in the left ventricular outflow tract. Six pigs were under general anesthesia equipped with transit time flow probes on their proximal aortas and Millar micromanometer catheters in their descending aortas to measure PWR, and Leycom conductance catheters in their left ventricles to measure SW. The PWR integral was calculated as the time integral of PWR per cardiac cycle. SW was calculated as the area encompassed by the pressure–volume loop (PV loop). The relationship between the PWR integral and SW was tested during extensive mechanical and pharmacological interventions that affected the loading conditions and myocardial contractility. The PWR integral displayed a strong correlation with SW in all pigs (R2 > 0.95, P < 0.05) under all conditions, using a linear model. Regression analysis and Bland Altman plots also demonstrated a stable relationship. A mixed linear analysis indicated that the slope of the SW-to-PWR-integral relationship was similar among all six animals, whereas loading and contractility conditions tended to affect the slope. The PWR integral followed SW and appeared to be a promising parameter for monitoring the energy transferred from the left ventricle to the aorta. This conclusion motivates further studies to determine whether the PWR integral can be evaluated using less invasive methods, such as echocardiography combined with a radial artery catheter.

BackgroundChanges in cardiac power parameters incorporate changes in both aortic flow and blood pressure. We hypothesized that dynamic and non-dynamic cardiac power parameters would track hypovolemia better than equivalent flow- and pressure parameters, both during spontaneous breathing and non-invasive positive pressure ventilation (NPPV).MethodsFourteen healthy volunteers underwent lower body negative pressure (LBNP) of 0, −20, −40, −60 and −80 mmHg to simulate hypovolemia, both during spontaneous breathing and during NPPV. We recorded aortic flow using suprasternal ultrasound Doppler and blood pressure using Finometer, and calculated dynamic and non-dynamic parameters of cardiac power, flow and blood pressure. These were assessed on their association with LBNP-levels.ResultsRespiratory variation in peak aortic flow was the dynamic parameter most affected during spontaneous breathing increasing 103 % (p < 0.001) from baseline to LBNP −80 mmHg. Respiratory variation in pulse pressure was the most affected dynamic parameter during NPPV, increasing 119 % (p < 0.001) from baseline to LBNP −80 mmHg. The cardiac power integral was the most affected non-dynamic parameter falling 59 % (p < 0.001) from baseline to LBNP −80 mmHg during spontaneous breathing, and 68 % (p < 0.001) during NPPV.ConclusionsDynamic cardiac power parameters were not better than dynamic flow- and pressure parameters at tracking hypovolemia, seemingly due to previously unknown variation in peripheral vascular resistance matching respiratory changes in hemodynamics. Of non-dynamic parameters, the power parameters track hypovolemia slightly better than equivalent flow parameters, and far better than equivalent pressure parameters.

This study assesses positional changes in cardiac power output and stroke work compared with classic hemodynamic variables, measured before and after elective coronary artery bypass graft surgery. The hypothesis was that cardiac power output was altered in relation to cardiac stunning. The study is a retrospective analysis of data from two previous studies performed in a tertiary care university hospital. Thirty‐six patients scheduled for elective coronary artery bypass graft surgery, with relatively preserved left ventricular function, were included. A pulmonary artery catheter and a radial artery catheter were placed preoperatively. Cardiac power output and stroke work were calculated through thermodilution both supine and standing prior to induction of anesthesia and again day one postoperatively. Virtually all systemic hemodynamic parameters changed significantly from pre‐ to postoperatively, and from supine to standing. Cardiac power output was maintained at 0.9–1.0 (±0.3) W both pre‐ and postoperatively and from supine to standing on both days. Stroke work fell from pre‐ to postoperatively from 1.1 to 0.8 J (P < 0.001), there was a significant fall in stroke work with positional change preoperatively from 1.1 to 0.9 J (P < 0.001). Postoperatively the stroke work remained at 0.8 J despite positional change. Cardiac power output was the only systemic hemodynamic variable which remained unaltered during all changes. Stroke work appears to be a more sensitive marker for temporary cardiovascular dysfunction than cardiac power output. Further studies should explore the relationship between stroke work and cardiac performance and whether cardiac power output is an autoregulated intrinsic physiological parameter.

Cardiac power, the product of aortic flow and blood pressure, appears to be a fundamental cardiovascular parameter. The simplified version named cardiac power output (CPO), calculated as the product of cardiac output (CO) in L/min and mean arterial pressure (MAP) in mmHg divided by 451, has shown great ability to predict outcome in a broad spectrum of cardiac disease. Beat‐by‐beat evaluation of cardiac power (PWR) therefore appears to be a possibly valuable addition when monitoring circulatory unstable patients, providing parameters of overall cardiovascular function. We have developed a minimally invasive system for cardiac power measurement, and aimed in this study to compare this system to an invasive method (ttPWR). Seven male anesthetized farm pigs were included. A laptop with in‐house software gathered audio from Doppler signals of aortic flow and blood pressure from the patient monitor to continuously calculate and display a minimally invasive cardiac power trace (uPWR). The time integral per cardiac cycle (uPWR‐integral) represents cardiac work, and was compared to the invasive counterpart (ttPWR‐integral). Signals were obtained at baseline, during mechanically manipulated preload and afterload, before and after induced global ischemic left ventricular dysfunction. We found that the uPWR‐integral overestimated compared to the ttPWR‐integral by about 10% (P < 0.001) in both normal hearts and during ventricular dysfunction. Bland–Altman limits of agreement were at +0.060 and −0.054 J, without increasing spread over the range. In conclusion we find that the minimally invasive system follows its invasive counterpart, and is ready for clinical research of cardiac power parameters.