Vascular Cardiac Compliance/Mechanics Flashcards
Differentiate compliance in Veins and arteries.
Arteries: Thick, muscular walls, low compliance (As V INC, P INC a lot)
Veins: Thin; More elastic; High compliance (As V INC, P INC very little)
Differentiate variables in Vascular Function vs Cardiac function curves.
• Vascular function curve: defines changes in central venous
pressure P v
that are caused by changes in cardiac output.
•Pv
is the dependent variable or response + cardiac output is the independent variable or stimulus.
• Cardiac function curve: Pv
or preload is independent variable
+ cardiac output is the dependent variable.
• Explains how cardiac output determines level of P
v
What is LaPlace’s Law?
- Describes Wall Tension of vessels
- T = [P x r]/ 2 x u
- Tension = Pressure x Radius / 2 x wall thickness
Ex. Deflated balloon harder to blow up
What is the Frank-Starling Curve?
- SV vs LVEDP
- Inc Afterload -> Shifts down and right
- DEC Afterload—> Shifts up and left
What is the Frank-Starling mechanism?
- Activated with increased preload (LVEDP)
- Compensates for reduction in SV caused by increased Afterload
How is the difference between Afterload fans preload utilized in treatment of heart failure?
- Pt given Vasodilators
- Vasodilators Increase SV by decreasing Afterload (Arterial pressure) + Decreasing ventricular preload
- Ventricular volume changes in response to decreased arterial pressure over several heart beats
How does reduced arterial pressure lead to an increase in SV?
• Initial end-diastolic volume EDV is 140 mL + end-systolic volume ESV is 80 mL.
• Reduced arterial pressure is reduced, ventricle can eject blood more rapidly,
stroke volume increases or difference between EDV and ESV increases and
ESV decreases
• Because less blood remains in ventricle after systole, ventricle does not fill to
same EDV found before afterload reduction.
• EDV or preload is “pulled along” secondarily + reduced as ESV decreases.
• Stroke volume increases because reduction in EDV is less than reduction in ESV.
What is Cor pulmonale?
- Pulmonary arterial HTN in Disease of lungs
- Results in R ventricular enlargement + R HF
How does doubling HR affect MVO2?
Doubles HR = Doble HVO2
How is Ventricular Wall Tension calculated?
- Similar to LaPlace’s Law
- Tension = [P x r]/ h
How does Aortic Stenosis affect the left ventricle?
- left ventricular pressure during ejection can be greater than aortic pressure.
- At given intraventricular pressure, wall stress and therefore afterload are increased by an
increase in ventricular inside radius or ventricular dilation.
What occurs due to ventricular hypertrophy?
Thickened wall + Reduced afterload
Permits more parallel muscle fibers or sarcomere units to share wall tension determined at given pressure + radius. Thicker wall is less tension experienced by each sarcomere unit.
How does aortic valve stenosis and ventricular dilation affect stroke volume?
- Both cause an increase in Aortic pressure and Systemic vascular resistance —> INC Afterload
- INC afterload —> INC ESV and Decrese in Stroke Volume
What affects
MVO2 more; Preload or afterload?
Afterload
Compare the increase in MVO2 of increasing SV vs other factors.
Increasing HR, aortic pressure AP, and inotropy Ino increase MVO 2 4x
more than equivalent percent change in stroke volume SV.