The degree of cerebral tissue saturation in heart failure has been proven to reflect functional capacity and disease severity and has potential prognostic value. Radon monitoring during exercise testing has clinical value. Cerebral tissue oxygen saturation measured by NIRS is simple and convenient.
This protocol-integrated NIRS into conventional CPET to increase the value of exercise testing in patients with heart failure. Demonstrating the procedure will be Yu Chen Liu, a technician from our laboratory. To begin this procedure, clean the patient's forehead twice with an alcohol pad to remove sweat and dirt from the skin.
Obtain large NIRS sensors in which the distance between the emitter and the detector is five cm and place the sensors on the forehead, bilaterally. Ensure that the sensors are securely attached. Next apply EKG electrodes to the anterior chest, bilateral acromioclavicular joints, and low back.
Have the patient sit on the bicycle ergometer and place the armband of the sphygmomanometer on them. Then, wear the mask of gas analysis for the patient place the sensors for the pulse oximeter on the patient's index finger. First, tell the patient to rest for at least two minutes to obtain a stable baseline value including the cerebral tissue oxygen saturation and respiratory exchange ratio.
Next, have the patient complete the warm-up stage on the cycle ergometer at a work rate of 10 watts for one minute. Increase the rate by 10 watts per minute then ask the patient to pedal at around 60 rpm until he fails to keep up with a cadence of over 50 rpm despite strong encouragement. Automatically average the cerebral tissue oxygen saturation value every second from the data scanned at a frequency of 100 Hz.Automatically measure the blood pressure every two minutes with the sphygmomanometer.
Analyze the gas component, breath-by-breath, including the oxygen uptake and the end-tidal carbon dioxide pressure. Then, have the patient complete the recovery stage at a work rate of zero watts for two to six minutes. In this study, both heart failure patients and healthy controls underwent cardiopulmonary exercise testing that incorporates cerebral tissue oxygen saturation monitoring by NIRS.
The cerebral tissue oxygen saturation values are seen to briefly be significantly lower in the heart failure group than in the control group. In the heart failure group, the cerebral tissue oxygen saturation at rest and at peak are linearly correlated with Brain Natriuretic Peptide, the peak oxygen uptake, and the oxygen uptake efficiency slope. Notably, the cerebral tissue oxygen saturation at rest is determined by the partial pressure of the end-tidal carbon dioxide at rest, hemoglobin, and mean arterial pressure at rest.
The procedure is simple and convenient. Patients with low cerebral saturation index warrent high medical attention. Integration of NIRS into CPET helps delineate the involvement of cerebral hemodynamic suppression causing exercise intolerance in patients with heart failure.
Besides its prognostic value, it needs longitudinal research to confirm.
