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_MS2 Cardio > 8/3- Cardiac Fct: Heart as a Pump > Flashcards

8/3- Cardiac Fct: Heart as a Pump Flashcards

1
Q

T/F: Preload is the ventricular volume before systole

A

True

Preload is the ventricular volume before systole

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2
Q

T/F: Afterload is measured after contraction starts

A

True

Afterload is measured after contraction starts

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3
Q

T/F: Wall stress is closely related to blood pressure

A

True

Wall stress is closely related to blood pressure

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4
Q

T/F: Starling’s law states that an increase in preload improves cardiac performance

A

True

Starling’s law states that an increase in preload improves cardiac performance

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5
Q

T/F: Decrease in afterload improves cardiac performance?

A

True

Decrease in afterload improves cardiac performance

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6
Q

T/F: The 3 key determinants of fiber shortening are preload, afterload, and contractility?

A

True

The 3 key determinants of fiber shortening are preload, afterload, and contractility

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7
Q

T/F: After a premature heart beat, the next beat is a stronger beat due to both better filling and better contractility?

A

True

After a premature heart beat, the next beat is a stronger beat due to both better filling and better contractility

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8
Q

T/F: During diastole, IVR occurs first and atrial kick last?

A

True

During diastole, IVR occurs first and atrial kick last

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9
Q

What side/chamber of the heart is this? Labels/Characteristics?

A

Right ventricle

  • Thin outer wall and septum
  • Concave outer RV wall moves towards septum in bellows-like action allowing thin-walled RV to eject large volume against low outflow P
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10
Q

What is the resultant circulatory change for the right ventricle? (pressure)

A

PA (pulmonary artery) pressure of 15-35 mmHg

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11
Q

Left ventricle characterized by ___ axis

A

Left ventricle characterized by long axis

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12
Q

Characteristics of LV contraction?

A
  • Decrease in chamber size and shortening of the long axis
  • Apex moves towards MV and closer to chest wall (causing PMI)
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13
Q

What is the resultant circulatory change for the left ventricle (pressure)?

A

Generate 100-120 mmHg AoP (aortic pressure) with each LV ejection

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14
Q

Where is the PMI?

A

Left MCL (mid-clavicular line) between 5th and 6th ribs

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15
Q

What are the determinants of cardiac function (5)?

A
  • Preload
  • Afterload
  • Wall stress
  • Contractility
  • Diastolic Function
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16
Q

What is preload? (def)

A

Blood volume in the ventricle at end-diastole

  • Preload is a key determinant of cardiac performance (CO and SV)
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17
Q

What is Frank Starling/Starling’s Law? Graph?

A
  • Peak tension developed by muscle increases as preload increases… within physiologic limits
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18
Q

What are the determinants of preload (4)?

A

- Intravascular volume*

- Venous return*

  • Atrial contraction
  • Pericardial function

(*most important)

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19
Q

What conditions involve increased intravascular volume (hypervolemia)?

A
  • Congestive heart failure
  • Renal failure
  • Overhydration
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20
Q

What conditions involve decreased intravascular volume (hypovolemia)?

A
  • Excessive Diuretics
  • Blood Loss
21
Q

What are the 3 main determinants of myocardial fiber shortening?

A
  • Preload
  • Afterload
  • Contractility
22
Q

Why is fiber shortening important for cardiac function?

A

Fiber shortening and ventricular size are key determinants of stroke volume (blood ejected with every heartbeat)

23
Q

What is afterload? (def)

A

Tension or force acting on ventricular fibers after onset of contraction or fiber shortening

24
Q

How do changes in afterload affect cardiac function?

A
  • BP elevation increases afterload and worsens fiber shortening and cardiac performance (SV and CO)
  • BP reduction decreases afterload and improves cardiac performance
25
Q

What is the effect of mitral regurgitation and perceived afterload of left ventricle? Ejection fraction?

A
  • Lower afterload

(- Greater ejection fraction too, based on change in volume)

26
Q

Increase/decrease in preload improves cardiac function?

A

Increase in preload improves cardiac function?

27
Q

Increase/decrease in contractility improves cardiac function?

A

Increase in contractility improves cardiac function

28
Q

Increase/decrease in afterload improves cardiac function?

A

Decrease in afterload improves cardiac function?

29
Q

In what clinical conditions is afterload important?

A
  • Increased afterload
  • Decreased afterload
  • Heart failure
30
Q

Examples of increased afterload?

A
  • Hypertension
  • Aortic stenosis

We call these conditions pressure overload conditions

31
Q

Examples of decreased afterload?

Effect on cardiac function?

A
  • Mitral regurgitation (“leaky” valve)
  • LV contracts against a lower afterload (LA) thus cardiac performance (EF) is improved!!!
32
Q

What happens to cardiac function after repair of MR?

A

Afterload is now higher(!) as the LV has to pump blood against the aorta ONLY rather than against lower pressure LA…

  • Thus EF and CO worsen after MR repair
33
Q

Which pt has higher cardiac performance?

A. Normal mitral valve

B. Mitral regurgitation

A

Which pt has higher cardiac performance?

A. Normal mitral valve

B. Mitral regurgitation

34
Q

In heart failure, CO and EF are high/low?

What happens when we reduce afterload with vasodilators?

A

In heart failure, CO and EF are low

When we reduce afterload with vasodilators (ACEI), CO and EF improve

  • Vasodilators are a key part of treatment of CHF
35
Q

Why is wall stress important?

A
  • Wall stress affects cardiac performance (adversely, just like afterload)
  • Wall stress affects MVO2
36
Q

What are the 3 main determinants of wall stress?

A
  • P (intracavitary pressure)
  • R (radius)
  • h (wall thickness)
37
Q

What equation is used to determine wall stress?

A

LaPlace Law

wall stress (WS) = PxR/2h

38
Q

What condition is shown here?

A

Eccentric hypertrophy

39
Q

What condition is shown here?

A

Concentric hypertrophy

40
Q

Which has increased wall stress? Why?

Which has decreased walls tress? Why?

A

Increased wall stress: left, due to marked increase in ventricle size

Decreased walls stress; right, due to marked increase in wall thickness

(recall LaPlace’s Law)

41
Q

Eccentric hypertrophy is a pathophysiologic result of what?

A

Volume overload

  • Mitral insufficiency
  • Atrial septal defect
42
Q

Concentric hypertrophy is a pathophysiologic result of what?

A
  • Hypertension
  • Aortic stenosis
43
Q

What is contractility?

A

Contractility and inotropic state refer to the INHERENT ability of muscle to contract INDEPENDENTLY of loading conditions

44
Q

Contractility vs. cardiac performance?

A

Contractility is load-dependent, unlike cardiac performance

45
Q

What is positive inotropic effect?

A

Positive inotropic effect- improvement in cardiac performance due to greater contractility in the absence of change in preload or afterload

46
Q

What is post-extrasystolic potentiation?

A

Contraction after a pause that follows a premature beat is more forceful than normal

  • Greater contractility and greater preload mediates stronger beat
47
Q

What are the 4 phases of diastole? graph

A
  • IVR
  • Rapid filling
  • Slow filling (diastasis)
  • Atrial kick
48
Q

What is compliance? graph

A

Increase in volume with little increase in pressure (shallower slope of pressure/volume curve)

49
Q

Cardiac Function: Key Points

  • Contrast preload & afterload
  • Frank-Starling: higher preload improves performance
  • Three key determinants of myocardial fiber shortening: preload, afterload & contractility; how do they do it?
  • Lower afterload in MR increases EF not contractility
  • LaPlace law: What are 3 determinants of wall stress?
  • Contrast contractility vs. cardiac performance
  • Define and explain post-extrasystolic potentiation

_MS2 Cardio (35 decks)

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