Ventricular Function Flashcards

1
Q

Equation for stroke volume?

A

SV = EDV - ESV

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2
Q

Equation for CO?

A

CO = HR x SV

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3
Q

Ventricular diastole begins with? Then what happens

A

Closure of the semilunar valves.
Followed by “isovolumic relaxation” that ends when atrial pressure > ventricular pressure.
“Rapid filling” with opening of AV valves.
“Reduced filling/diastasis”, with a length determined by HR.

Terminated by atrial systole

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4
Q

How can you observe the effect of diastolic filling. Draw

A

Ventricular P-V relationship. Non-linear and passive. Drawn

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5
Q

Draw systolic P-V relationship

A

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6
Q

Draw the complete ventricular P-V loop

A

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7
Q

Four Determinants of ventricular performance

A

1) Preload
2) Afterload
3) Inotropic state
4) Heart rate

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8
Q

Preload is?

What happens as it increases

A

The degree of filling (EDV), and the stretch of muscle before contraction
-determines filament overlap (L-T relationship)

As it increases: SV increases, maximal potential pressures increases (FS mechanism!)

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9
Q

Afterload is?

A

Pressure at which valve opens. Pressure against which ventricle contracts (P in aorta, MAP)

  • Systolic LV pressure or aortic pressure a main determinant.
  • Fibre tension/myocyte stress is also important

Incr afterload > incr preload > decr SV

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10
Q

Inotropic state.

A

ABility of myocardium to contract with given preload/afterload. Force of contraction

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11
Q

Easiest way to measure preload?

A

To use LV (EDP) as a measure. It’s really hard to measure actual volumes

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12
Q

Systemic hypertension an example of

A

increased afterload. SV actually decreases

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13
Q

Wall stress (tension/thickness) is proportional to…?

A

(P x r / thickness)

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14
Q

ventricular filling is the portion most affected by changed chronotropy, circle this on an ECG. Why is this most affected?

A


The force of contraction increases as HR increases.
BUT with a high HR, SV is reduced due to reduced filling time.

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15
Q

R-R interval? How is this affected by HR?

A

Time for complete cardiac cycle. As HR increases this interval steadily decreases

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16
Q

How is time for Isovolumic contraction/relaxation affected by changing HR

A

It isn’t. remains very steady

17
Q

Diastolic interval? How does this change?

A

Time for ventricular filling. Greatly reduced as HR increases

18
Q

Balance of the Left and Right sides of the heart

A
  • No matter the changes, as the system is closed, both sides of the heart pump the same volume OVER TIME.
  • So changes affect BOTH sides.
  • Balance is affected by arrhythmias
19
Q

Bc heart is a balanced system, increased afterload >

A

> > increased preload

  • inc P in aorta > inc LV afterload
  • initially dec LV V
  • RV continues pumping
  • Blood accumulates in lungs
  • inc stretch of capacitance circuit
  • Filling P to LV inc
  • Next beat LV EDV increases (preload)
  • SV increases
20
Q

Draw the closed system and an example of the things in it that affect

A

21
Q

Factors that affect Preload

A

MANY! Blood volume, venous tone, posture, HR, atrial contraction

These will ALL affect the amount of blood loaded into the ventricles during the diastolic phase

22
Q

Factors that affect Afterload

A
  • Hypertension
  • Vasoconstriction
  • Aortic stenosis (narrowed valve)
  • LV geometry
  • Heart failure
23
Q

Factors that affect Chronotropic State

A

Neural (ANS)
Catecholamines (eg PKA)

increased HR= + chronotropic state
Decreased HR = - chronotrpic state

24
Q

How do we assess Ventricular function

A
We look at the 
Ejection fraction (55-75%)
Peak dP/dt
End-systolic PV relation
Ventricular function curves
25
Q

Ejection fraction equation, and how it’s determined

A

EF% = (EDV-ESV) / EDV x 100

Usually determined from echocardiogra or cardiac MRI data

Normal EF (LV): 55-60% at rest, to 85% during exercise

Depressed contractility if EF

26
Q

max rate (dP/dt) of LV pressure is used as an indicator of contractility

A

+ during contraction
- during relaxation

The steeper the gradient, the faster the rate of pressure increase. THat’s why its more positive/narrow during systole as the pressure increase is faster then relaxation phase

27
Q

End systolic P-V relation

A

The gradient is a boundary line for ESV. Ventricular function can be measured from the gradient

+ inotropic stimulus: Gradient steeper

  • inotropic stimulus (eg heart disease, less pressure/force can be generated) : shallow gradient
28
Q

LV EDP indication of

A

EDV, just easier to measure

29
Q

Stroke WOrk

A

Work performed each cardiac cycle to eject blood under pressure into the aorta and pulmonary artery.

SW = P(MAP) x SV
or
SW = integral of P x volume change (dV) estimated by MAP x SV

30
Q

Altered inotropic state changes?

A

End-systolic PV relationship and therefore the maximum pressure that can be developed

31
Q

An increased HR leads to

A

Increased CO (CO = HR x SV)
Increased inotropic state
Decreased SV due to reduced filling tome