From the Research
Squatting increases right ventricular afterload by elevating systemic vascular resistance, as evidenced by the most recent study on the topic 1. When a person squats, blood from the lower extremities is compressed and redirected toward the central circulation, increasing venous return to the right heart. This augmented preload initially increases right ventricular output, but simultaneously, the compression of abdominal and pelvic vessels raises systemic vascular resistance. The increased resistance creates higher pressure in the pulmonary circulation that the right ventricle must pump against, thus elevating right ventricular afterload. This hemodynamic change is particularly relevant in certain cardiac conditions, such as:
- Hypertrophic cardiomyopathy, where squatting can temporarily improve symptoms by increasing afterload and reducing outflow tract obstruction
- Pulmonary hypertension or right heart failure, where the increased afterload from squatting may worsen cardiac function and symptoms The physiological mechanism involves both mechanical compression of vessels and autonomic nervous system responses that regulate vascular tone and cardiac output during postural changes, as discussed in the context of right ventricular loading by lung inflation during controlled mechanical ventilation 1. Key factors influencing right ventricular afterload include:
- Pulmonary vascular resistance (PVR)
- Pulmonary arterial compliance (PAC)
- Characteristic impedance, with perturbations in nitric oxide metabolism playing a crucial role in the evolution of increased afterload 2
- The impact of squatting on right ventricular afterload is also related to the concept of RV-PA coupling, which depicts the interaction between RV contractility and afterload, as well as the invasive and non-invasive techniques for its assessment 3.