Pressure-Volume Loops Flashcards
pressure-volume relationship
*for normal hearts, the pressure-volume relationship sits slightly to the left of the optimal actin-myosin overlap
*as such, most hears have a reserve with which they can increase their forward flow when needed, usually with stimulation of the sympathetic nervous system
*y-axis: LV pressure (mmHg)
*x-axis: LV volume (mL)
end-diastolic pressure-volume relationship (EDPVR)
*determined by the relaxation ability of the heart (note: lusitropy = relaxation)
*it determines the amount of blood that can fill the ventricle at a given pressure
*notice, it is not a straight line; the pressure-volume changes based on the amount of blood in the LV during diastole
end-systolic pressure-volume relationship (ESPVR)
*determined by the contractile state of the heart (note: inotropy = contractility)
*it determines the LV pressure generated and the amount of blood left in the LV after contraction (at the end of systole)
left ventricle pressure-volume relationship loop
*systole occurs when the LV muscle is contracting; starts with MV closure and ends with AV closure
*diastole occurs when the LV muscle is relaxing after contraction and filling with blood; coincides from AV closure to MV closure
steps of the cardiac cycle, in terms of pressure/volume
1) LV FILLING: mitral valve opens when LV pressure < LA pressure → volume & pressure of LV are increasing
2) ISOVOLUMETRIC CONTRACTION: mitral valve closes once LV pressure > LA pressure → pressure of LV increases rapidly (volume remains the same)
3) SYSTOLIC EJECTION: aortic valve opens once LV pressure > aortic pressure → volume & pressure of LV decreases (blood is being ejected from LV)
4) ISOVOLUMETRIC RELAXATION: aortic valve closes once enough blood has been ejected → pressure of LV plummets (volume remains the same)
5) mitral valve opens when LV pressure < LA pressure (CYCLE REPEATS: GO BACK TO STEP 1)
EDV & ESV and diastolic & systolic blood pressures - location of LV PVR
*end-diastolic volume (EDV): where the mitral valve closes
*diastolic blood pressure: where the aortic valve opens
*systolic blood pressure: peak of the curve where the aortic valve is opening and the blood is being ejected from LV
*end-systolic volume (ESV): where the mitral valve opens
Wigger’s Diagram
*plots LV, aorta, and left atrial pressure against time
LV stroke work =
stroke work = stroke volume x MAP
recall: stroke volume = EDV - ESV
cardiac work =
cardiac work = stroke work x heart rate
recall: stroke work = stroke volume x MAP
2 important things to recognize with heart failure and pressure-volume relationships
- heart failure often has increased left ventricular end-diastolic pressure
- heart failure often has decreased left ventricular stroke volume
primary change - defined
the immediate, direct impact of the change
secondary change - defined
the additional changes noted after 20 cardiac cycles (20 heartbeats) have completed
increased contractility: PVR primary change
*increased contractility increases stroke volume (and LV EF) by reducing LV end-systolic volume as a result of improved LV muscle function/efficiency
*SIMPLE: increased SV, decreased ESV, increased LV EF
*factors that can increase contractility: isoproterenol, dobutamine, digoxin, sympathetic stimulation, increased intra-cellular calcium
decreased contractility: PVR primary change
*decreased contractility decreases stroke volume (and LV EF) by increasing LV end-systolic volume as a result of worsened LV muscle function/efficiency
*SIMPLE: decreased SV, increased ESV, decreased LV EF
*factors that can decrease contractility: MI, myocarditis, cardiomyopathy, calcium channel blocker
LV compliance/stiffness
*compliance = volume/pressure
*stiffness (elastance) = pressure/volume
*as LV EDV increases, the LV becomes less compliant
*as LV EDV increases, the LV EDP increases
increase in relaxation/lusitropy: PVR primary change
*an increase in relaxation will result in a lower LV EDP
*SIMPLE: decreased LV EDP
*factors that increase relaxation: exercise, sympathetic stimulation (short-term)
decrease in relaxation/lusitropy: PVR primary change
*a decrease in relaxation will result in a higher LV EDP
*SIMPLE: increased LV EDP
*factors that decrease relaxation: ischemia, anything that impairs the cell’s ability to remove calcium at the end of cardiac contraction
preload - overview
*stretch on the LV wall at the end of diastole (LV filling) immediately before the LV starts to contract
*best described by end-diastolic LV wall stress
increased preload: PVR primary change
*as preload increased, LV end-diastolic pressure increases and LV end-diastolic volume increases
*SIMPLE: increased EDV, increase EDP, increased stroke volume
*factors that increase preload: IV fluids, squatting, venoconstriction, exercise
decreased preload: PVR primary change
*as preload decreases, LV end-diastolic pressure decreases and LV end-diastolic volume decreases
*SIMPLE: decreased EDV, decreased EDP, decreased stroke volume
*factors that decrease preload: IV diuresis, nitroglycerin, valsalva/standing
afterload - overview
*stretch on the LV wall at the end of systole (LV contracting) immediately before the LV starts to relax
*best described by end-systolic LV wall stress
increased afterload: PVR primary change
*as afterload increases, LV end-systolic volume increases (more blood in LV) and LV stroke volume decreases
*SIMPLE: increased ESV, decreases stroke volume
*factors that increase afterload: IV pressors, handgrip, aortic stenosis, hypertension
decreased afterload: PVR primary change
*as afterload decreases, LV end-systolic volume decreases (more blood leaves LV during systole) and LV stroke volume increases
*SIMPLE: decreased ESV, increased stroke volume
*factors that decrease afterload: ACE inhibitors/ARBs, beta-2 stimulation, IV nitroprusside, alpha-1 blockade
