Hemodynamics of left ventricular support devices and left ventricular pressure-volume loop Flashcards
Placement of IABP
It is placed just distal to the left subclavian artery (at the level of the tracheal carina fluoroscopically) and extends down proximal to the renal arteries
Timing of IABP inflation and deflation
Inflation - early diastole, at or just before the dicrotic notch
-increases the coronary perfusion in cardiogenic low-output states but cannot increase coronary flow across critical coronary stenoses
Deflation - beginning of systole; just at the isovolumic contraction phase
-this creates a negative pressure in the aorta that sucks flow from the LV, thus reducing afterload and myocardial wall stress
Identify
A. Unassisted diastole
B. Unassisted systole
C. Timing of inflation
D. Diastolic augmentation
E. Assisted end diastolic pressure
F. Assisted systolic pressure
It inflates at the _______________, which corresponds to the dicrotic notch and beginning of diastole and deflates at the _________________, which corresponds to the beginning of the isovolumic contraction
- End of T wave
- Peak of R wave
IABP increases cardiac output by _______ , up to 0.5 to 1 L/min and decreases LV filling pressure and PCWP by _______
~20%
~20%
Contraindications to IABP
Moderate to severe AR
HOCM
The IABP is contraindicated in moderate or severe AI and HOCM (since intracavitary obstruction increases with afterload reduction).
Relative CI: severe PAD
Effects of
1. Late deflation and early inflation
2. Late inflation and early deflation
- Late delfation/early inflation - Balloon inflated in systole increases afterload
- Late inflation/early deflation - Suboptimal increase in coronary perfusion and suboptimal sucking effect
It is a microaxial rotatory pump that expels blood from the LV to the aorta.
Impella 2.5 or 5.0
Impella 2.5 can provide up to 2.5 L/min of flow support or Impella 5 can provide up to 5 L/min of support
Impella reduces the end-diastolic volume (preload) and the end-systolic volume (wall tension or afterload), which reduces O2 demands. The subsequent reduction in end-diastolic pressure improves subendocardial perfusion and microcirculatory flow.
Impella reduces afterload differently from IABP: the former reduces LV volume, whereas the latter reduces aortic resistance.
Contraindications to Impella device
Moderate or severe AS (AVA <1.5 cm2)
Moderate or severe AI
HOCM
VSD
Presence of LV thrombus
Relative CI: severe PAD
LA-to-iliac artery bypass consisting of an extracorporeal pump that withdraws blood from the left atrium
TandemHeart
TandemHeart is an LA-to-iliac artery bypass consisting of an extracorporeal pump that withdraws blood from the left atrium via a 21F transseptal canula inserted through a femoral vein. Blood is then pumped into the iliac artery (15F-17F cannula) at a continuous flow rate of up to 3.5 L/min (15F outflow cannula) or 5 L/min (17F outflow cannula)
pLVAD unloads the LV and improves subendocardial perfusion, with a potential for more cardiac output increase than Impella 2.5
TandemHeart indirectly unloads the LV, is less effective in reducing afterload, and, therefore, less effective in reducing O2 consumption
Impella 2.5 is likely more suited for high-risk PCI or MI not accompanied by shock, where ischemic protection is the primary concern, whereas TandemHeart is likely more suited for cardiogenic shock, where hemodynamic support is the primary concern.
This corresponds to the tension the myocardium is pumping against during systole, called ventricular wall tension
Ventricular afterload
Afterload depends on the intracavitary systolic pressure but also the intracavitary size, that is, the intracavitary stretch (the more the myocardium is stretched, the higher the tension against the myocardial wall).
Laplace formula
Laplace law = systolic LV radius × systolic LV transmural pressure / 2× myocardial thickness
The more the myocardium is stretched, the higher the tension against the myocardial wall
At a given pressure, wall stress and therefore afterload increase when the ventricle further dilates
Afterload also depends on the ventricular wall thickness. The thicker the wall, the less tension is experienced by each sarcomere unit. Note that the RV is more afterload dependent than the normal LV because the RV is thinner than the LV.
Diuresis reduces preload and reduces afterload by ______________
Positive pressure ventilation reduces preload and reduces afterload by reducing __________________ (pericardial pressure being positive in case of positive pressure ventilation).
Reducing systolic LV radius
LV transmural pressure
Identify
A - Diastole
B - Preload
C - EDPV Relationship (chamber stiffness)
D - ESPV Relationship (contractility)
E - Afterload
F - Systole
G - IVC
H - IVR
I - SV
J - Stroke Work
Identify
Systolic LV failure
The contractility is decreased; thus, the end-systolic line goes down. The chamber stiffness is reduced in chronic heart failure; thus, the stiffness curve is shifted to the right (ie, LV end-diastolic pressure remains low for a high end-diastolic volume). In case of decompensated failure, the preload is severely increased so that the end-diastolic volume is on the steep portion of the diastolic pressure-volume line, contractility is reduced, and afterload is increased (blue loop). The loop is narrow (low stroke volume).
After diuresis and afterload-targeted therapies, preload and afterload are reduced and stroke volume is increased (dashed blue loop). Changes in afterload more strikingly affect stroke volume than changes in preload.
Identify
Diastolic LV failure
The diastolic pressure-volume relationship is shifted up, so that end-diastolic pressure is increased even for a normal end-diastolic volume (ie, increased LVEDP despite normal LV volume) (blue loop). Contractility is unchanged. After therapy (preload and afterload reduction), the pressure-volume loop is shifted to the left (dashed blue loop). Adding a drug with lusitropic (relaxant) effect will shift the diastolic pressure relationship down (eg, calcium channel blocker) (blue arrow).
Identify
Effect of IABP
IABP reduces afterload and thus increases stroke volume, without significantly affecting preload. Although the LV is unloaded, it is ejecting a higher volume so that the stroke work (loop area) is unchanged, but the potential energy and the O2 consumption are reduced. Myocardial contractility may also improve as a result of improved coronary microcirculation and reduced demands.
Identify
Effect of Impella or TandemHeart support device
Preload and afterload are both reduced. The intrinsic stroke volume and cardiac output are reduced; however, the total cardiac output is increased as a result of the active pumping. The stroke work and the total pressure-volume area are reduced, and thus, the O2 consumption is reduced.
Identify
Mitral Stenosis
The following describes changes that occur in the left ventricular pressure-volume (PV) loop when there is mitral stenosis. Mitral stenosis (red PV loop in figure) impairs left ventricular filling, which reduces in end-diastolic volume (preload). This leads to a decrease in stroke volume (reduced width of PV loop) by the Frank-Starling mechanism and a fall in cardiac output. Reduced ventricular filling and reduced aortic pressure decrease ventricular wall stress (afterload), which may cause a small decrease in ventricular end-systolic volume. However, this does not offset the reduction in end-diastolic volume. Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume (shown as the width of the loop) decreases.
Identify
Aortic Stenosis
The following describes changes that may occur in the left ventricular pressure-volume (PV) loop in the presence of chronic aortic stenosis. In aortic stenosis (red loop in figure), left ventricular emptying is impaired because of high outflow resistance caused by a reduction in the valve orifice area when it opens. This high outflow resistance causes a large pressure gradient to occur across the aortic valve during ejection, such that the peak systolic pressure within the ventricle is increased. This leads to an increase in ventricular wall stress (afterload), a decrease in stroke volume (width of PV loop), and an increase in end-systolic volume compared to normal (black loop). Stroke volume decreases because the velocity of fiber shortening is decreased by the increased afterload (see force-velocity relationship). Despite the elevated end-systolic volume, the end-diastolic volume usually decreases because, over time (years, decades), the ventricle wall becomes thicker (hypertrophied). This increases ventricular stiffness (decreases compliance), which causes a large elevation in end-diastolic pressure despite reduced filling. Although the stroke volume is reduced, the end-diastolic volume is also reduced and therefore the ejection fraction does not decrease significantly. This represents a condition of heart failure with preserved ejection fraction (HFpEF), or diastolic dysfunction.
Identify
The following describes changes that occur in the left ventricular pressure-volume loop when there is chronic mitral regurgitation. In mitral valve regurgitation (red loop in figure), as the left ventricle contracts, blood is not only ejected into the aorta but also back into the left atrium. This causes left atrial volume and pressure to increase abnormally during ventricular systole. Note in the pressure-volume loop that there is no true isovolumetric contraction phase (no vertical line between mitral valve closure and aortic valve opening) because blood flows across the mitral valve and back into the atrium as soon as ventricular pressure exceeds left atrial pressure. Regurgitation continues after aortic valve opening. The net effect is that the ventricular stroke volume (EDV-ESV; width of loop) is increased.
There is no true isovolumetric relaxation (vertical lines between aortic valve closure and mitral valve opening) because when the aortic valve closes and the ventricle begins to relax, the mitral valve is not completely closed, so blood continues to flow back into the left atrium (therefore further decreasing ventricular volume) as long as intraventricular pressure is greater than left atrial pressure. During ventricular diastolic filling, the elevated pressure within the left atrium is transmitted to the left ventricle during filling so that the left ventricular end-diastolic volume and pressure increase. Ventricular end-diastolic volume is also increased because in chronic mitral regurgitation the ventricle anatomically dilates (remodels) over years and decades. This increases the ventricular compliance. Increased end-diastolic volume would cause wall stress (afterload) to increase if it were not for the reduced outflow resistance and peak systolic pressure. The net effect of these changes is that the width of the pressure-volume loop is increased (i.e., ventricular stroke volume is increased); however, ejection into the aorta (forward flow) is reduced. The increased ventricular “stroke volume” (end-diastolic minus the end-systolic volume) in this case includes the volume of blood ejected into the aorta and the volume ejected back into the left atrium.
Identify
The following describes changes that occur in the left ventricular pressure-volume loop when there is aortic regurgitation. In aortic valve regurgitation (red loop in figure), the aortic valve does not close completely at the end of systolic ejection. As the ventricle relaxes during diastole, blood flows from the aorta back into the ventricle, so the ventricle immediately begins to fill from the aorta (before filling from the left atrium). Therefore, there is no true phase of isovolumetric relaxation (no vertical line between aortic valve closure and mitral valve opening) because as the ventricle relaxes, even before the mitral valve opens, blood is entering the ventricle from the aorta, thereby increasing ventricular volume. Once the mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because aortic pressure is higher than ventricular pressure during diastole. This augments ventricular filling so that end-diastolic volume is increased as shown in the pressure-volume loop. Ventricular end-diastolic volume is also increased because in chronic aortic regurgitation the ventricle anatomically dilates (remodels), which increases ventricular compliance.
When the ventricle begins to contract and develop pressure, blood is still entering the ventricle from the aorta because aortic pressure is higher than ventricular pressure; therefore, there is no true isovolumetric contraction because volume continues to increase. Once the ventricular pressure exceeds the aortic diastolic pressure, the ventricle ejects blood into the aorta. The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, ventricular peak (systolic) pressure, and stroke volume (as shown by the increased width of the pressure-volume loop). If the ventricle is not in failure, end-systolic volume may only be increased a small amount (as shown in figure) due to the increased afterload (ventricular wall stress). If the ventricle goes into systolic failure, then end-systolic volume will increase by a large amount and the peak systolic pressure and stroke volume and net forward flow into the aorta will fall.
