Hemodynamics is the core of each hemodialysis treatment. Cardiac index (CI) is still a big unknown in clinical medicine and clinicians rely on changes in blood pressure to assess CI, which is less sensitive. Besides blood pressure, CI is also critically determined by peripheral resistance. The Transonic HD03 monitor allows us to directly measure CI and make inferences of cardiac function.
All nephrologists agree that cardiovascular mortality is by far the most common cause of death in HD patients. It is important that this cardiovascular mortality is mostly related to heart failure and small vessel disease leading to sudden death or systolic failure.
Echocardiography is central to detect cardiac dysfunction; cardiac biomarkers are also useful to identify patients with an increased risk. Optimal fluid and blood pressure control are essential to reduce cardiac strain.
We have been focusing on prognostic associations of biomarkers so far and found the powerful significance of spuriously elevated cardiac troponins in the risk assessment of HD patients. Now we are focusing on hemodynamic parameter measured with the Transonic HD 03 monitor.
We conducted a prospective study with 215 patients which so far is the greatest study in this field. During follow-up we will identify those hemodynamic parameters that are prognostically relevant. We are also in touch with Transonic to derive novel hemodynamic parameters from the recordings that might add valuable data.
Identification of reduced CI could prompt a bundle of measures to improve cardiac function aiming at improving long-term outcome. On a level of a single HD treatment, monitoring of CI could prevent a critical drop that might induce cardiac injury, referred to as cardiac stunning.
The standard Transonic monitor measures primarily access flow (AF) and helps detect patients with absolutely high access flow (AF > 2.0 l/min). The HD03 monitor helps to additionally measure cardiac output (CO). Knowing the CO of a patient with high AF enables to check if the high flow is still compensated by an adequate increase in CO. That would be reflected by a AF/CO ratio of < 20%, which is the value a normal flow AF. However, if the ratio exceeds 30% of the CO, there is no adequate cardiac compensation anymore. These patients could have an absolute AF of
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