Wide Pulse Pressure in Aortic Insufficiency
In chronic severe aortic insufficiency, wide pulse pressure results from the combination of elevated systolic blood pressure (due to increased total stroke volume ejection) and reduced diastolic blood pressure (due to rapid diastolic runoff back into the left ventricle), creating the characteristic bounding peripheral pulses and hemodynamic signature of this volume overload state. 1, 2
Pathophysiologic Mechanisms
Chronic Aortic Insufficiency
The left ventricle responds to chronic AR with compensatory mechanisms including increased end-diastolic volume, enhanced chamber compliance, and combined eccentric-concentric hypertrophy, allowing ejection of a large total stroke volume to maintain forward flow. 1 This adaptation creates the hemodynamic profile:
Elevated systolic pressure occurs because the LV must eject both the normal forward stroke volume plus the regurgitant volume that leaked back during the previous diastole, resulting in systolic hypertension even when systemic vascular resistance is normal 1, 2
Reduced diastolic pressure develops as blood rapidly runs off from the aorta back into the LV throughout diastole, causing progressive decline in aortic diastolic pressure 1, 2
The combination produces wide pulse pressure (difference between systolic and diastolic pressures), which accounts for the peripheral physical findings such as bounding pulses, water-hammer pulse, and other classic signs 2
Acute Aortic Insufficiency Differs Markedly
In acute severe AR, pulse pressure may NOT be increased because systolic pressure is reduced (due to decreased forward stroke volume from the unprepared LV) and aortic diastolic pressure equilibrates with the rapidly elevated LV diastolic pressure. 1 This represents a critical diagnostic pitfall:
The sudden regurgitant volume imposed on a normal-sized LV that cannot acutely dilate results in dramatically elevated LV end-diastolic pressure 1
Forward stroke volume decreases because the ventricle operates on the steep portion of its pressure-volume relationship without compensatory chamber dilatation 1
Systolic blood pressure falls while diastolic pressure equilibrates between aorta and LV, potentially masking the severity of regurgitation on physical examination 1
Clinical Implications
Hemodynamic Consequences
The afterload excess caused by systolic hypertension in chronic AR leads to progressive LV dilation and eventual systolic dysfunction if untreated. 2 The wide pulse pressure reflects:
- Increased transaortic stroke volume (normal forward flow plus regurgitant volume) 2
- Enhanced LV preload from volume overload 1
- Elevated systolic wall stress despite normal systemic vascular resistance 1
Diagnostic Considerations
Severe AR is associated with wide pulse pressure such that systolic blood pressure is higher than in patients without AR even when systemic vascular resistance is normal. 1 Important caveats:
Transaortic stroke volume increases further with medications that lower heart rate (like beta blockers), which may paradoxically appear to increase blood pressure 1
Vasodilating drugs (ACE inhibitors, ARBs) reduce systolic blood pressure without substantially reducing diastolic pressure in chronic AR because they don't affect heart rate 1
In acute AR, many characteristic physical findings of chronic AR are modified or absent, leading to potential underestimation of severity 1
Management Relevance
The goal of vasodilator therapy in chronic AR is to achieve significant decrease in systolic arterial pressure, which reduces the afterload excess and may delay progression. 2 However:
There is no evidence that vasodilating drugs reduce AR severity or alter disease course in patients without systemic hypertension 1
Recommendations for hypertension management apply to patients with chronic asymptomatic AR as for the general population 1
In acute severe AR, beta blockers should be used very cautiously if at all because they block the compensatory tachycardia needed to maintain cardiac output 1