Vascular Cardiac Compliance/Mechanics Flashcards

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1
Q

Differentiate compliance in Veins and arteries.

A

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)

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2
Q

Differentiate variables in Vascular Function vs Cardiac function curves.

A

• 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

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3
Q

What is LaPlace’s Law?

A
  • 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

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4
Q

What is the Frank-Starling Curve?

A
  • SV vs LVEDP
  • Inc Afterload -> Shifts down and right
  • DEC Afterload—> Shifts up and left
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5
Q

What is the Frank-Starling mechanism?

A
  • Activated with increased preload (LVEDP)

- Compensates for reduction in SV caused by increased Afterload

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6
Q

How is the difference between Afterload fans preload utilized in treatment of heart failure?

A
  • 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
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7
Q

How does reduced arterial pressure lead to an increase in SV?

A

• 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.

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8
Q

What is Cor pulmonale?

A
  • Pulmonary arterial HTN in Disease of lungs

- Results in R ventricular enlargement + R HF

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9
Q

How does doubling HR affect MVO2?

A

Doubles HR = Doble HVO2

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10
Q

How is Ventricular Wall Tension calculated?

A
  • Similar to LaPlace’s Law

- Tension = [P x r]/ h

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11
Q

How does Aortic Stenosis affect the left ventricle?

A
  • 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.
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12
Q

What occurs due to ventricular hypertrophy?

A

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.

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13
Q

How does aortic valve stenosis and ventricular dilation affect stroke volume?

A
  • Both cause an increase in Aortic pressure and Systemic vascular resistance —> INC Afterload
  • INC afterload —> INC ESV and Decrese in Stroke Volume
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14
Q

What affects

MVO2 more; Preload or afterload?

A

Afterload

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15
Q

Compare the increase in MVO2 of increasing SV vs other factors.

A

Increasing HR, aortic pressure AP, and inotropy Ino increase MVO 2 4x
more than equivalent percent change in stroke volume SV.

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16
Q

What is the main target of drugs which reduce coronary artery disease?

A
  • Decrease afterload
  • Decrease HR
  • Decrease Inotropy
17
Q

Why. Must CAD patients comply with anti-hypertensive medications?

A

Hypertension increases MVO2 due to increased afterload