Effect of Peripheral Vascular Resistance on Preload and Afterload
Yes, increasing peripheral vascular resistance increases both preload and afterload, with afterload being more significantly affected than preload. 1
Mechanism of Increased Afterload
Afterload is primarily defined as the wall stress during systolic ejection and is a key determinant of ventricular function. When peripheral vascular resistance (PVR) increases:
- Wall stress increases due to higher intracavitary pressure against which the ventricle must contract 1
- According to the law of LaPlace, wall stress (afterload) is directly proportional to intracavitary pressure and ventricular diameter 1
- Systemic vascular resistance increases, creating greater impedance to ventricular ejection 1
- Arterial elastance increases, which worsens ventriculo-arterial coupling 1
The right ventricle is particularly sensitive to changes in afterload, with minor increases causing large decreases in stroke volume due to its shallower end-systolic pressure-volume relationship compared to the left ventricle 1.
Mechanism of Increased Preload
Preload is affected by peripheral vascular resistance through several mechanisms:
- Increased peripheral resistance reduces forward flow, causing blood to "back up" in the venous system 1
- This increases mean circulatory filling pressure (MCFP), as demonstrated in experimental studies 2
- Higher venous pressure translates to increased end-diastolic volume and pressure in the ventricles 1
- The increased right atrial pressure that results from higher PVR and RV afterload imposes back pressure on venous return 1
Clinical Implications
The relationship between PVR, preload, and afterload has important clinical implications:
In heart failure, increased PVR contributes to both preload and afterload elevation, worsening ventricular function 1
Vasodilator therapy in heart failure works by reducing both preload and afterload 3
Different vasodilators have varying effects:
- Nitrates primarily reduce preload through venodilation
- Hydralazine predominantly reduces afterload through arteriolar dilation
- Nitroprusside, phentolamine, and prazosin produce balanced arterial and venous dilation 3
Increased afterload from elevated PVR can lead to ventricular dilation, which promotes valvular regurgitation and drives ventricular interdependence 1
Physiological Nuances
Several important physiological nuances should be considered:
- The right ventricle is more sensitive to afterload changes than the left ventricle 1
- Ventriculo-arterial coupling becomes inefficient when PVR increases acutely, requiring more energy expenditure to maintain adequate cardiac output 1
- Late-systolic load has a particularly strong influence on early diastolic relaxation 4
- Increased PVR can reduce coronary perfusion by increasing end-diastolic pressure, potentially inducing subendocardial ischemia 1
In summary, increased peripheral vascular resistance affects both preload and afterload through direct hemodynamic effects, with afterload being more immediately and significantly affected. This relationship is fundamental to understanding cardiovascular pathophysiology and the therapeutic approach to conditions like heart failure.