Does an increase in Pulmonary Vascular Resistance (PVR) increase both afterload and preload?

Effect of Increased Pulmonary Vascular Resistance on Afterload and Preload

An increase in Pulmonary Vascular Resistance (PVR) primarily increases right ventricular afterload, while its effect on preload is more complex and can lead to increased right-sided preload but decreased left-sided preload. 1

Hemodynamic Effects of Increased PVR

Effect on Afterload

When PVR increases, there are several important hemodynamic consequences:

1. Direct increase in RV afterload:

   • PVR is a major component of right ventricular afterload 1
   • Higher PVR requires the right ventricle to generate greater pressure to maintain forward flow 1
   • The RV is particularly sensitive to increases in afterload, with even minor increases causing large decreases in stroke volume 1

2. Mechanisms of afterload increase:

   • Increased resistance across the pulmonary microvasculature 1
   • Development of West zone 2 conditions (when pleural pressure exceeds pulmonary venous pressure) 1
   • Alveolar pressure becomes the outflow pressure for the RV, further increasing afterload 1

3. RV response to increased afterload:

   • Unlike the LV, the RV has a shallower end-systolic pressure-volume relationship 1
   • This results in greater changes in end-systolic volume with smaller changes in pressure 1
   • The RV is poorly adapted to handle pressure increases compared to volume changes 1

Effect on Preload

The effect of increased PVR on preload is more complex:

1. Right-sided preload effects:

   • Increased RV afterload leads to RV dilation 1
   • RV dilation promotes tricuspid regurgitation 1
   • Right atrial pressure increases as a result of higher RV afterload 1
   • This creates a "back pressure" on venous return, potentially increasing right-sided preload 1

2. Left-sided preload effects:

   • Reduced RV stroke volume from increased PVR leads to decreased LV filling 1
   • This effectively reduces left ventricular preload 1
   • Ventricular interdependence further complicates this relationship 1

Ventricular Interdependence

A critical aspect of the PVR-preload relationship involves ventricular interdependence:

1. Mechanical interactions:

   • Forces are directly transmitted between ventricles through the myocardium and pericardium 1
   • RV dilation causes leftward shift of the interventricular septum 1
   • This increases LV end-diastolic pressure while reducing LV transmural filling pressure 1

2. Diastolic competition:

   • Ventricles compete for filling space within the confined pericardial space 1
   • As the RV dilates due to increased PVR, it impedes LV diastolic filling 1

Clinical Implications

The relationship between PVR, afterload, and preload has important clinical implications:

1. RV failure progression:

   • Increased PVR leads to RV dilation and eventual RV failure 2
   • As PVR rises, pulmonary arterial pressure initially increases but may later fall as RV function declines 1

2. Therapeutic considerations:

   • Treatments that reduce PVR can improve RV-pulmonary arterial coupling 3
   • Pulmonary arterial capacitance (PAC) may be a better predictor of outcomes than PVR alone 4
   • Both proximal and distal pulmonary arterial stiffening contribute to increased RV afterload 5, 6

Common Pitfalls in Understanding PVR Effects

1. Oversimplification of afterload:

   • PVR alone incompletely describes RV afterload 1
   • Pulsatile components and wave reflection also contribute significantly 3

2. Misunderstanding preload effects:

   • Assuming increased PVR uniformly increases preload in all chambers
   • Failing to account for ventricular interdependence effects

3. Neglecting the time course:

   • Acute vs. chronic PVR increases have different compensatory mechanisms
   • Initial compensation may mask the severity of RV afterload increase

In summary, increased PVR directly increases RV afterload, which can increase right-sided preload due to back pressure effects while simultaneously decreasing left-sided preload due to reduced RV output and ventricular interdependence.