Demonstration of Knowledge and Evidence

DKE #1 (Group 1): Knowledge of the heart rate, stroke volume, cardiac output, blood pressure, and oxygen consumption responses during sub-maximal and maximal exercise.

Keywords: heart rate, stroke volume, cardiac output, blood pressure, oxygen consumption, submaximal exercise, and maximal exercise

Kinetics of Cardiac Output at the Onset of Exercise in Precapillary Pulmonary Hypertension (PH) is a research article from the Biomed Research International. This study consisted of fifteen participants; five pulmonary hypertension participants and ten healthy controls that performed a submaximal exercise in a supine position on a cycle ergometer. The hypothesis is that the ‘beat-by-beat description of CO kinetics upon exercise onset in precapillary PH would be slower than those of healthy subjects but no study has been conducted to observe maximal exercises responses.

To begin with, Precapillary Pulmonary Hypertension is a hemodynamic condition that is caused by an increase in pulmonary vascular resistance (PVR) leading to right ventricular failure. PVR is associated with patients who have a tolerant exercise capability to handle an increase in workload. With that happening, this can be due to the compression of the left ventral that is dilated by the right ventricle (RV), causing limited physiological functions in the increase of stroke volume before exercise, therefore, altering the response of cardiac output (CO). One way to assess cardiac output is thermodilution (TD), which determines the steady-state parameter. TD is non-invasive and is an accurate measure of CO on the arterial pulse pressure wave, for patients with pulmonary hypertension and healthy patients.

The study consisted of five patients with precapillary pulmonary hypertension (four with pulmonary arterial hypertension, and 1 with chronic thromboembolic pulmonary hypertension) and ten healthy control patients were collected. Throughout the study, patients provided an informed consent form. Patients with pulmonary hypertension proceeded with a right heart catheterization (RHC) to measure the pulmonary artery mean pressure, pulmonary artery wedge pressure, right atrial pressure, COPD, and systemic vascular resistance as a mean arterial pressure. Cardiac output is measured by the Thermodilution and Modelflow. In which COPD and COMF were determined by the 10ml injection of ice-cold sterile, isotonic glucosamine solution through the catheter’s lumen following a noninvasive procedure recording of the arterial pulse pressure by the Portapres system. The mean values were calculated using beat-by-beat numerical values over a 1-minute steady-state, rest, and after a 2-minute exercise. Before exercise, the hemodynamic testing patients were set to place their feet on the ergometers pedals causing a five-minute delay in hemodynamic stabilization from a new set steady state. Participants with pulmonary hypertension began the exercise starting by peddling at 60 RPM at 20 watts, and the healthy controls peddled with 50 watts for five minutes. The workload performed by the two groups was later determined by the mean increase in heart rate reserve (HRR) obtained from the steady pulse. Furthermore, pulmonary hypertension patients that performed the exercise displayed a decrease in stroke volume and cardiac output onset of exercise between 20 to 30 seconds.

Results show that patients in the healthy group displayed an increase at the beginning of exercise reaching a new steady state, whereas pulmonary hypertension patients cardiac output decreased between three to five beats, stabilizing 20 seconds during the exercise thus, reaching a new steady state level. The healthy control group displayed a decrease in heart rate on the onset of exercise but the change was not seen in pulmponary hypertension participants. Also, assessing cardiac output in pulmonary hypertension patients using beat-by-beat kinetics displaced a decrease in response at a supine position on the cycle ergometer, making the hypothesis statistically significant. Before the decrease in cardiac output on the onset of exercise, there was a drop in stroke volume. This study assessed five patients with pulmonary hypertension, concluding that there was no significant increase in stroke volume because the increase in cardiac output during exercise triggered specific heart rate parameters. Heart rate kinetics responses were seen to be slower in the healthy group rather than the pulmonary hypertension group. Additionally, these changes were also seen on set exercises within individuals with the pulmonary vascular disease, heart failure, and healthy subjects. The researchers stated that there are no studies that show decreases in cardiac output on the onset of exercise. With a sudden drop in cardiac output, this means that the decline in stroke volume illustrates that the hemodynamic changes in the residual volume do not accept enough venous return causing impairment in pulmonary hypertension patients.

Overall, the researchers have concluded that since there was a limited number of participants in the study, the submaximal work results between pulmonary hypertension patients and the healthy group may have triggered the measurement of kinetics, heart rate, stroke volume, and cardiac output parameters. If patients performed maximal test during this study this would allow a direct measure of oxygen consumption, max heart rate, and the amount of carbon dioxide during the test. This is the first study conducted using beat-by-beat kinetics, indicating that heart rate, stroke, volume, and cardiac