Cardiac output and index

The heart is actually a muscular hydraulic pump that may generate pressure in addition to flow. It consists of a pump (the guts) and tubes (arteries) that generate energy. Cardiac output is the flow through this closed circuit, which is influenced by cardiac contractility and the multifaceted interaction between vascular resistance, flow compliance, filling pressures, and total intravascular volume. The pumping capability of the guts is defined as cardiac power output (CPO) (Yildiz et al., 2017). CPO can be a direct correlate of end-organ perfusion (Mishra, 2016). This hemodynamic measurement uses the physical fluid rule: power = pressure x flow and is the product of concurrently measured cardiac output (or cardiac index) and mean arterial pressure (Fincke et al., 2004).

Formulas (Yildiz et al., 2017)

• Resting CPO is measured in watts using the next formula: cardiac output (L/min) x mean arterial pressure divided by 451. CPO < 0.6 W indicates hemodynamic compromise and is related to an increased risk of mortality.
• Resting Cardiac Power Index (CPI) is measured in watts per square meter (W/m²) using the next formula: Cardiac index (L/min/m²) x mean arterial pressure divided by 451. Normal CPI is 0.5-0.7 W/m².

Under the umbrella of CPO are three subcategories, which include maximal CPO, reserve CPO, and resting CPO. Maximal CPO and reserve CPO may be measured noninvasively or invasively during cardiopulmonary stress testing. When there’s cardiac (or pump) dysfunction, whether as a result of myocardial infarction, valvular heart disease, myocarditis, etc., maximal and reserve CPO decrease to levels that cause impairment of resting CPO. Deficiencies in maximal and reserve CPO manifest as symptoms of exercise intolerance, similar to exertional dyspnea. Severe decreases in resting CPO may be seen in patients with advanced heart failure and/or cardiogenic shock (Yuldiz et al., 2017).

You may wonder how this data is useful or relevant to the care of a cardiac patient. Well, here’s why! Invasive hemodynamic monitoring, namely right heart catheterization, has been used for a long time to risk stratify and guide medical therapy in patients with heart failure and/or cardiogenic shock. The primary focus has been on measurements of pulmonary capillary wedge pressure (PCWP) and cardiac output, and while adjusting therapy to enhance these parameters has improved patient symptoms, it has not consistently improved overall patient outcomes. Remarkably, none of those hemodynamic measurements captured the essence of cardiac contractility, meaning that PCWP is a measure of intracardiac output, while cardiac output or index is a measure of cardiac output. It has been recognized that these measurements don’t truly reflect the synergistic nature of our cardiac system, which consists of an energy source (the guts) and its conduits (arteries) that conduct that energy throughout the body. Therefore, the true pumping power of the guts is more accurately reflected by measurements of cardiac output and index (Fincke et al., 2004).

The utility of CPO and CPI has been the topic of much research. Below is a brief list of a few of these studies, including crucial information:

• Fincke et al (2004) studied 541 patients with cardiogenic shock and located that CPO was the strongest independent predictor of in-hospital mortality. Patients with CPO ≤ 0.53 W had a 58% likelihood of in-hospital mortality.
• George et al (2012) found CPO to be a reliable discriminator compared with other hemodynamic measures in predicting successful left ventricular assist device (LVAD) weaning and explantation. They reported that every one patients with CPO > 1.1 W experienced myocardial recovery and tolerated LVAD explantation.
• Grodin et al. (2015) studied 495 patients with advanced heart failure and located that lower resting CPI was related to higher left and right filling pressures and abnormal cardiorenal biomarkers. Their study showed that CPI < 0.44 W/m² was related to an increased risk of hostile outcomes (mortality, heart transplantation, and left ventricular assist device implantation). They concluded that the CPI is a reliable prognostic measure and support its use in risk stratification in patients with advanced heart failure.
• Yildiz et al (2017) studied 172 patients with advanced heart failure who were referred for heart transplantation. They hypothesized that resting CPO would correlate with survival. They found that indeed, resting CPO < 0.54 W was an independent predictor of poor outcomes on this patient population.

Cardiac output and index are hemodynamic parameters that provide insight into the present clinical status of patients with cardiogenic shock or advanced heart failure and are strong predictors of patient prognosis. Look for these measurements to turn out to be a part of the every day clinical dialogue in your facility when caring for patients with these critical diagnoses.

Fincke, R., Hochman, J. S., Lowe, A. M., Menon, V., Slater, J. N., Webb, J. G., LeJemtel, T., .Cotter, G., & SHOCK Investigators (2004). Cardiac output is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. (2), 340-348. https://doi.org/10.1016/j.jacc.2004.03.060

George, J.K., Shabari, F.R., Abdul-JAbbar, A.H., Gazzala, J., Rossell, G., Odegaard, P., Segura, A., Delgado, R.M. (2012). Cardiac power output predicts myocardial recovery and successful left ventricular assist device explantation. (4S), S74. https://doi.org/10.1016/j.healun.2012.01.197

Grodin, J. L., Mullens, W., Dupont, M., Wu, Y., Taylor, D. O., Starling, R. C., Wilson, W. H. (2015). Prognostic role of cardiac power index in outpatients with advanced heart failure. (7), 689-696. https://doi.org/10.1002/ejhf.268

Mishra, S. (2016). Scaling up ventricular assist devices for decompensated heart failure: device selection and timing. , S1-S4. https://doi.org/10.1016/j.ihj.2015.12.012

Yildiz, O., Gamze, A., Zumrut, D.T., Yenigun, C.D., Yazicioglu, N. (2017). Evaluation of resting cardiac power output as a prognostic think about patients with advanced heart failure. (6), 973-979. https://doi.org/10.1016/j.amjcard.2017.06.028