From the Guidelines
Inspiration increases afterload in the left ventricle, while its effect on the right ventricle is more complex, involving decreased afterload during positive airway pressure and increased afterload during negative intrathoracic pressure. The effect of inspiration on afterload is multifaceted, depending on the specific conditions of ventilation and the state of the heart and lungs. According to the study by 1, changes in pleural pressure (Ppl) and transpulmonary pressure (TP) during mechanical ventilation have significant hemodynamic effects. When Ppl decreases during spontaneous inspiratory efforts, it effectively lowers the pressure baseline of the heart relative to the rest of the body, increasing the gradient for the return of blood to the right ventricle (RV). However, this decrease in Ppl also increases left ventricular (LV) afterload because the heart needs more force to maintain normal arterial pressure.
Key points to consider:
- The decrease in Ppl during inspiration increases LV afterload due to the increased pressure gradient the left ventricle must pump against to eject blood into the aorta.
- Positive airway pressure, on the other hand, decreases LV afterload but can decrease venous return to the RV and eventually to the LV, thereby having little benefit for cardiac output.
- The right ventricle is more sensitive to afterload than to variations of preload, and its afterload can be significantly affected by changes in alveolar pressure and Ppl.
- In conditions like ARDS, the acutely injured lung has a reduced capacity to accommodate flowing blood, and increased permeability can lead to fluid filtration and edema formation, further complicating the effects of inspiration on afterload.
In clinical practice, understanding these complex interactions is crucial for managing patients with heart failure or those requiring mechanical ventilation. As noted in 1, minimizing intrathoracic positive pressure ventilation and correcting acidosis can improve LV filling in the setting of RV failure. Additionally, the use of vasodilators or other medications to reduce afterload can be beneficial in specific cases, as discussed in 1.
Overall, the effect of inspiration on afterload is nuanced and depends on various factors, including the method of ventilation, the patient's underlying cardiac and pulmonary conditions, and the specific hemodynamic parameters being considered.
From the Research
Effect of Inspiration on Cardiac Afterload
- The effect of inspiration on cardiac afterload is a complex phenomenon that involves various physiological mechanisms 2, 3, 4, 5.
- Spontaneous inspiration can increase left ventricular afterload, while mechanical ventilation with positive pressure can reduce it 3.
- The respiratory pump can improve cardiovascular functions, including greater cardiac filling and output, when a "sweet spot" for generation of negative intrathoracic pressure during inspiration can be maintained at or less than 10 cmH2O below normal inspiration 2.
- Respiratory effort during inspiration changes right ventricular preload and afterload, with inspiration improving systolic emptying of a larger end diastolic volume and increasing the ejection fraction 4.
- The right ventricle is highly sensitive to small loading changes during inspiration, and both RV preload and afterload are altered during inspiration, either in spontaneous breathing or during mechanical ventilation 5.
Key Findings
- Increased intrathoracic pressure during inspiration can result in adverse hemodynamic effects, including increased cardiac afterload 2, 3.
- The use of mechanical ventilation can have both positive and negative effects on cardiac afterload, depending on the mode of ventilation and the pre-existing cardiac and respiratory status 3.
- The assessment of right ventricular function during inspiration is crucial, as it can be affected by various factors, including venous return, pulmonary arterial pressure, and pulmonary vascular resistance 4, 5.
- Pulse pressure variations, central venous pressure, and echocardiography can be used to monitor right ventricular function in abnormal clinical situations 5.