14. Cardiac Output & Contractility Flashcards

1
Q

what is preload

A
  • amount of blood ready to be pumped at the end of diastole = end diastolic volume
  • wall tension in ventricle just before contraction is initiated
  • fiber length at the end of diastole
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2
Q

how is preload related to venous return

A

more blood returning → greater preload

  • in a steady state, venous return = CO
  • frank starling: volume of blood ejected depends on the volume present at end of diastole
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3
Q

what is afterload

A

force opposing contraction, pressure required to eject blood (i.e. open aortic/pulmonary valve)

  • increase in vessel pressure causes and increase in afterload
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4
Q

how does afterload effect the velocity of muscle fiber contraction?

when is velocity the greatest?

A
  • velocity of shortening decreases as afterload increases (inverse relationship)
  • greatest if afterload were 0
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5
Q

what effect does preload have on contractility and CO?

afterload?

A

↑ preload → ↑ CO and contractility

↑ afterload → ↓ CO
Heart must then ↑ contractility or HR to overcome

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6
Q

Describe the relationship between heart rate and contractility in terms of the positive staircase effect.

A

↑ HR (+ chronotropic effect) → ↑ contractility (+ ionotropic effect)

Positive staircase effect: ↑ force of contraction in a stepwise manner d/t cumulative increase in intracellular Ca; more Ca enters cell and more is taken up into SR

also seen with premature or out of synch beat; weak beat will be followed by stronger beats

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7
Q

how do you calculate SV and what is normal

A

SV: volume of blood ejected by ventricles with each beat
= HR x CO = EDV - ESV

Normal = 70 mL

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8
Q

how do you calculate EF% and what is normal

A

Ejection fraction: fraction of EDV ejected in each SV, measures efficiency and contractility
= SV / EDV

Normal = 55%, reduced in heart failure patients

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9
Q

how do you calculate CO and what is normal

A

CO: total volume of blood ejected by ventricle per minute
= SV x HR

Normal = 5L/min

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10
Q

what effects does the sympathetic system have on contractility?

how?

A

positive ionotropic effect through B1 adrenergic activation → ↑ in contractility

Activation causes phosphorylation of…

  • Sarcolemmal Ca channels → ↑ inward ICa during phase 2
  • Phospholamban (stimulatory) → ↑ activity of Ca pump so more Ca is accumulated in the SR
  • Troponin I (inhibitory, inhibition of inhibitor)
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11
Q

what effect do cardiac glycosides have on contractility?

how?

A

Cardiac glycosides: ↑ contractility

Done by inhibiting Na-K-ATPase → ↑ in intracellular Na, diminishing gradient used by Na-Ca exchanger (more Ca stays in)

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12
Q

what effect does the parasympathetic system have on contractility?

how?

A

negative ionotropic effect in atria only via muscarinic activation → ↓ in contractility

  • ↓ inward ICa during phase 2
  • ACh ↑ outward IK via K-ACh channel
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13
Q

what is happening between points 1 and 2 on pressure volume loop?

A

1 → 2: isovolumetric contraction, all valves closed

  • 1: EDV (preload), marks the end of diastole, pressure is low (EDV = 140 mL)
  • 2: afterload, marks point where ejection of blood begins, aortic valve open
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14
Q

what is happening between points 2 and 3 on pressure volume loop?

A

2 → 3: ventricular ejection

  • max pressure between points 2 and 3
  • SV = 70 mL (measured by width of loop)
  • 3: ESV
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15
Q

what is happening between points 3 and 4 on pressure volume loop?

A

3 → 4: isovolumetric relaxation

  • 3: systole ends (ESV) and ventricles relax
  • Pressure falls quickly by volume remains constant
  • 4: AV valve opens
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16
Q

what is happening between points 4 and 1 on pressure volume loop?

A

4 → 1: ventricular filling

17
Q

what effect does increased preload have on pressure volume loop?

A

↑ venous return, ↑ blood volume → ↑ EDV

Shifts point 1 and 2 to the right

Compensation: ↑ contractility

18
Q

what effect does increased afterload have on pressure volume loop?

A

↑ in aortic pressure (ventricle must eject blood against higher pressure) → ↓ SV, ↓ EF%
↓ SV → ↑ ESV

Shifts point 2 and 3 up

d/t aortic stenosis, hypertension

19
Q

what effect does increased contractility have on pressure volume loop?

A

greater tension in ventricle → ↑ SV, ↑ EF% (↑ SV → ↓ ESV)

Shifts points 3 and 4 to the left, 2 → 3 gets higher

d/t adrenergic stimulation

20
Q

what is stroke work and how does it effect function of the heart?

A

= SV x pressure work (aortic pressure)

Area within the pressure-volume loop

Heart has to work harder to overcome aortic pressure → cardiomegaly

21
Q

how does pressure work effect LV?

what does this have to do with O2 consumption?

how do you calculate CO based on O2 consumption

A
  • LV must proportionally work harder than RV despite CO being similar because systemic pressure is greater than pulmonary pressure.
  • Pressure work (fighting aortic pressure) requires the most O2 consumption
  • CO = O2 consumption / ([O2] pulmonary a - [O2] pulmonary v)

Aortic stenosis and HTN increase LV pressure work

22
Q

describe the cardiac function curve

A

↑ venous return → ↑ RA pressure → ↑ EDV and end diastolic fiber length

23
Q

describe the vascular function curve

A

relationship between venous return and RA pressure

24
Q

what is the equilibrium point between the cardiac and vascular function curve

A

CO = 5 L/min

RA pressure = 2 mm Hg

25
Q

what effect will increased inotropy have on the cardiac fxn curve?

decreased?

A

↑ ionotropy → ↑ HR → ↓ afterload

↓ ionotropy → ↓ HR → ↑ afterload

26
Q

what is mean systemic pressure

A

pressure in atria when there is no blood flow

CO and VR are zero, pressure is equal throughout cardiovascular system

27
Q

how would mean systemic pressure be increased and what effect would this have on the graph?

decreased?

A

↑ MSP by ↑ in blood volume or ↓ in venous compliance
- shifts curve to the right

↓ MSP by ↓ in blood volume or ↑ in venous compliance
- shifts curve to left

28
Q

what effect does + inotropy have on cardiac fxn and how would this appear on the graph?

  • inotrophy?
A

+ inotropic effect: ↑ contractility and CO

  • slope of cardiac fxn curve ↑
  • e.g. digitalis
  • inotropic effect: ↓ contractility and CO
  • slope of cardiac fxn curve ↓
29
Q

what effect does increased TPR have on cardiac fxn and how would this appear on the graph?

decreased TPR?

A

Increased: ↓ CO and venous return
- Shifts intersection point ↓

Decreased TPR: ↑ CO and venous return
- Shifts intersection point ↑

***No change in atrial pressure

30
Q

what effect does increased blood volume have on cardiac fxn and how would this appear on the graph?

decreased blood volume?

A

↑ blood volume: ↑ MSP, ↑ CO and RA pressure
- cardiac function curve moves up

↓ blood volume: ↓ MSP, ↓ CO and RA pressure
- cardiac function curve moves down

31
Q

what happens to inotropy, vascular compliance, blood volume, and TPR in heart failure?

A

↓ inotropy and vascular compliance

↑ blood volume and TPR