Description
- Ventricular pressure–volume loops depict the relationship between pressure and volume in the left ventricle (LV). They aid with assessment of preload, contractility, and afterload as well as other physiologic parameters.
- Commonly used techniques to acquire this data include left heart catheterization (direct measurements) and pulmonary artery catheters (extrapolation).
- The pressure–volume relationship delineates a single cardiac cycle. This is comprised of four basic phases:
- Phase a (Points 4–1): Ventricular filling: Begins with the mitral valve open and blood from the left atrium passively enters the ventricle. This is followed by the atrial kick and ends with mitral valve closure.
- Phase b (Points 1–2): Isovolumetric contraction: Begins with the mitral and aortic valve closed and contraction without ejection of blood. It ends with aortic valve opening.
- Phase c (Points 2–3): Ejection: Begins with the aortic valve open and blood being propelled into the systemic circulation. It ends with aortic valve closure. Note that electromechanical diastole begins during ejection of blood from the aorta; the ventricle begins to relax and the aortic valve does not close until the LV pressure drops below aortic pressure.
Phase d (Points 3–4): Isovolumetric relaxation: Begins with the mitral and aortic valve closed and relaxation of the ventricle without a change in volume. It ends with mitral valve opening.
- Preload is depicted by the end diastolic volume (EDV; Point 1).
- Afterload is represented by the pressure at the end of isovolumetric contraction (Point 2).
- Inotropy can be assessed by the end-systolic pressure–volume relationship (ESPVR). The ESPVR curve becomes steeper and shifts to the left as inotropy (contractility) increases.
Stroke volume is represented by the difference between the EDV and end-systolic volume (ESV).
- Left ventricular compliance is depicted by the reciprocal of the slope seen at end-diastole (Point 1); this is called the end-diastolic pressure–volume relationship (EDPVR).
- Stroke work (SW) describes the work performed by the ventricle to eject the stroke volume into the aorta. It can be assessed by the area within the pressure–volume loop or pressure–volume area (PVA) (Points 1–4). This combines the external stroke work (SW) with the potential energy (PE) remaining at the end of systole. Myocardial oxygen consumption can be estimated by the PVA (recall that the primary determinants of VO2 are preload, afterload, and contractility).
- The ventricle is best described as an ellipsoid shape and its volume is best described by the geometric formula V = 4/3
r3, where r is the radius.
Physiology/Pathophysiology
- Systolic dysfunction signifies a loss of inotropy.
End-diastolic volume (preload): Increase
- ESV: Increase
- Stroke volume: Decrease
- Inotropy: Decrease; ESPVR slope decreases and shifts rightwards
- Compliance: A dilated ventricle will exhibit an increase; EDPVR slope will decrease and shift rightward
- Afterload: for any given afterload, there is a decreased velocity of fiber shortening
- Stroke work: Decreased
- Tension: Increase
Diastolic dysfunction signifies a decrease in ventricular filling secondary to hypertrophy or impaired relaxation (decreased lusitropy).
- End-diastolic volume (preload): Decrease
- ESV: Decrease or no change
- Stroke volume: Decrease
- Inotropy: No change or increases
- Compliance: Decrease; EDPVR slope will increase
- Afterload: Increases when secondary to hypertrophy
- Stroke work: Decreased secondary to a decrease in stroke volume
- Tension: Decrease
- Aortic stenosis (AS): The narrowing of the LVOT requires the LV to generate a much higher pressure in order to create an adequate stroke volume per each ventricular contraction. The amount of pressure that the LV must generate to create an adequate stroke volume is dependent on the degree of stenosis and the flow rate across the valve. Chronically, the total coronary flow increases in proportion to the increased LV wall stress and mass, but eventually, adequate subendocardial flow becomes difficult to attain leading to ischemia.
- End-diastolic volume (preload): Increases acutely
- ESV: Increase (to a greater extent than EDV)
- Stroke volume: Decrease
Inotropy: Increases; slope of ESPVR increases and shifts leftward
- Compliance: Decreases; slope of EDPVR increases secondary to the left ventricular hypertrophy that is typically associated with AS
- Afterload: Increase
- Stroke work: Decrease
- Tension: Increase
- Mitral stenosis (MS) is marked by the pathologic obstruction of flow from the left atrium to the LV. This obstruction results in elevated LA pressure and pulmonary pressures. There is a decrease in stroke volume secondary to a decrease in end-diastolic volume (preload). This decrease in preload leads to a decrease in cardiac output (CO) and aortic pressure, particularly aortic diastolic pressure.
- Aortic regurgitation (AR), also known as aortic insufficiency (AI), is caused by the aortic valve not closing at the end of systolic ejection which allows blood to flow back from the aorta to the LV during the diastolic relaxation. As a result, there is no true LV isovolumic relaxation because blood is flowing back into the LV before the mitral valve even opens.
- End-diastolic volume (preload): Increase
- ESV: Initially, mild increase or no change; with failure, significant increase
- Stroke volume: Initially, increase in stroke volume; if the ventricle goes into systolic failure, there is a decrease
- Inotropy: Mild decrease or no change; does not change significantly in the chronic state
Compliance: Increase; slope of EDPVR decreases and shifts rightward
- Mitral regurgitation (MR) results in blood from the LV entering the left atrium during ventricular systole. This results in an increase in the LA's volume and pressure during ventricular systole. There is no true isovolumetric contraction phase because as soon as the LV pressure exceeds LA pressure, blood flows backwards across the mitral valve and into the atrium. Additionally, there is no true isovolumetric relaxation because as the aortic valve closes and the ventricle relaxes, the MV remains open and blood flows back into the LA. This leads to an even smaller ventricular volume.
- End-diastolic (preload): Increase
- ESV: Small decrease or no change
- Stroke volume: "Increase;" this is because the loop accounts for both the blood ejected forward into the aorta as well as the blood ejected back into the left atrium
- Inotropy: No change or mild decrease
- Compliance: Increases; the slope of EDPVR decreases and shifts rightward
- Afterload: Decrease
- Stroke work: Increase
Tension: Decrease
- Aortic stenosis
- Prevent hypotension
- Prevent events that decrease CO
- Maintain normal sinus rhythm
- Avoid tachycardia and bradycardia
- Mitral stenosis
- Maintain heart rate slightly lower to allow sufficient time in diastole and flow across the MV
- Avoid atrial fibrillation in order to maintain the atrial kick
- Carefully titrate fluid administration in order to avoid volume overload
- Aortic regurgitation
- Maintain HR >80 beats/min to avoid increased diastolic time and therefore LV overload
- Avoid an increase in systemic vascular resistance (SVR)
- Treat acute overload with vasodilators
- Mitral regurgitation
- Prevent events that would decrease CO
- Maintain normal to fast heart rate
- Afterload reduction
- Maintain adequate preload
P × R)/2 h; where T is tension,