Education
PV Loop Changes During Cardiac Abnormalities
- Dilated Cardiomyopathy
The ventricle becomes highly dilated without appreciable thickening of the wall. The LV may be unable to pump enough blood to meet the body’s demands.
The end systolic and diastolic volumes increase and the pressures remain relatively unchanged. The ESPVR and EDPVR curves are shifted to the right.
- Left Ventricular Hypertrophy
This is an increase in the mass (and sometimes size) of the ventricle. This could be a normal reversible response to cardiovascular conditioning or an abnormal irreversible response to chronically increased volume load (preload) or increased pressure load (afterload).
The thickening of the ventricular muscle results in decreased compliance. As a result, LV pressures are elevated, the EDV is increased and the ESV is decreased, causing an overall reduction in cardiac output.
- Restrictive cardiomyopathy
Restrictive cardiomyopathy includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
This condition occurs when heart muscle is gradually infiltrated or replaced by scar tissue or when abnormal substances accumulate in the heart muscle. The ventricular systolic pressure remains normal, diastolic pressure is elevated and the cardiac output is reduced.
- Valve Diseases
Aortic stenosis
Aortic stenosis is abnormal narrowing of the aortic valve. This results in the LV pressures being much greater than the aortic pressures during LV ejection. The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve.
Severe aortic stenosis results in
- reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity)
- increased end-systolic volume
- compensatory increase in end-diastolic volume and pressure
Mitral stenosis
This is a narrowing of the mitral valve orifice when the valve is open. Mitral stenosis impairs LV filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume by the Frank-Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume. Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume decreases.
Aortic regurgitation (aortic insufficiency)
This is a condition in which the aortic valve fails to close completely at the end of systolic ejection, causing leakage of blood back through the valve during LV diastole.
The constant backflow of blood through the leaky aortic valve implies that there is no true phase of isovolumic relaxation. The LV volume is greatly increased due to the enhanced ventricular filling.
When the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure), implying that there is no true isovolumic contraction. Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.
The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, LV systolic pressure, and stroke volume.
Mitral regurgitation
This occurs when the mitral valve fails to close completely, causing blood to flow back into the left atrium during ventricular systole.
The constant backflow of blood through the leaky mitral valve implies that there is no true phase of isovolumic contraction. Since the afterload on the ventricle is reduced, end-systolic volume can be smaller than normal.
There is also no true isovolumic relaxation because some LV blood flows back into the left atrium through the leaky mitral valve. During ventricular diastolic filling, the elevated atrial pressure is transmitted to the LV during filling so that LV end-diastolic volume (and pressure) increases. This would cause the afterload to increase if it were not for the reduced outflow resistance (due to mitral regurgitation) that tends to decrease afterload during ejection. The net effect of these changes is that the width of the PV loop is increased (i.e., ventricular stroke volume is increased). However, ejection into the aorta (forward flow) is reduced. The increased ventricular stroke volume in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium.