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Cardiovascular MBCHB2 > Lecture 16: Ventricular function > Flashcards

Lecture 16: Ventricular function Flashcards

1
Q

What happens to ventricular volume at the VE/IVR time period and why? (wiggers diagram)

A

Ventricular volume becomes negative as their is negative flow (backwards) because E aorta is less than E ventricle. (some back flow)

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2
Q

How can the phases filling and ejection be divided in the wiggers diagram?

A

Into rapid and reduced time periods.

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3
Q

What is the general difference between left and right ventricles in terms of pressures and valve sequences?

A

Pressure is lower in the right ventricle therefore timing is slightly different.

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4
Q

Describe the timing of the mitral and tricuspid valves

A

The tricuspid valve opens before the mitral

The tricuspid valve closes after the mitral

i.e LV has less filling time

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5
Q

Describe the timing of the aortic and pulmonary valve

A

The pulmonary valve opens before the aortic valve

The pulmonary valve closes after the aortic

i.e LV has less ejection time

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6
Q

Why do the AV and semilunar valves have different timings between the left and right sides of the heart?

A

RV valves open sooner and close later because:

  • Differences in electrical activation and pressures (takes less time to generate pressure in the RV.)
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7
Q

Describe the pressure of the RA

A

~3mmHg

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8
Q

Describe RV pressures

A

(s) 18mmHg

d) 0mmHg (i.v.r

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9
Q

Describe PA pressures

A

(s) 18mmHg

(d) 12mmHg

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10
Q

Describe PA wedge pressures (cap)

A

8mmHg average

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11
Q

Describe LA pressures

A

8 mmHg average

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12
Q

Describe LV pressures

A

(s) 130 mmHg

(d) 0 mmHg

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13
Q

Describe the systemic aortic pressure

A

(s) 130 mmHg

(d) 75 mmHg

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14
Q

Whats the components of CO?

A

CO = HR x SV

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15
Q

What are the determinants of SV?

A
  • Preload
  • Afterload
  • Inotropy
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16
Q

How does HR affect CO?

A

HR directly influences CO and also indirectly acts via the determinants of SV particularly preload and inotropic state.

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17
Q

Describe the main factors of CO;

A

CO = SV x HR

SV = EDV - ESV

EDV influenced by Preload
ESV influenced by Afterload and Inotropic state

HR influences preload and Inotropic state

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18
Q

How does HR influence preload?

A

Reduced preload by reducing the time of ventricular filling therefore redoing SV

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19
Q

How does HR influence inotropic state?

A

HR relates to the force frequency relationship that plays a minor role in ionotropy.

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20
Q

What are the relavant graphs for ventricular performance?

A 
PV loop
Ejection Fraction
Peak dP/dT
Ventricular function curve
CO/VR MRAP curve a.k.a guyton VP graph
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21
Q

What does the linear line on the P-V graph represent?

A

Potential pressure of the chamber

This is never achieved as the valves open once threshold pressure is reached

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22
Q

Potential pressure increases linearly with and represents what relationship?

A

EDV

This clearly reflects the force-sarcomere length relationship.

23
Q

When is the length tension relationship for sarcomeres exhibited?

A

During isometric or fixed length muscle contraction

24
Q

Why can sarcomeres generate varying levels of tension at a fixed resting length?

A

Inotropic state accounts for this and means that sarcomeres can generate more force from an unchanged resting length

25
Q

What can be obtained from a P-V loop?

A

The ventricular work performed each cardiac cycle (stroke work)

SW = SV x TPR (P xV)

26
Q

What are the four determinants of cardiac performance?

A

Preload
Afterload
Inotropic state
Chronotropic state

27
Q

What is preload?

A

The tension produced by the degree of stretch of myocyte filaments

  • L-T relationship
  • Length dependant activation
    (a) - Increased stretch increases troponin C sensitivity to Ca
    (b) - Increased stretch increases the activation of stretch sensitive Ca channels
28
Q

What is Afterload?

A

The pressure of which the ventricle must pump against

Increased in hypertension.

29
Q

What is inotropic state?

A

The degree of activation of contractile proteins by Ca in the myocyte sarcomere.

30
Q

What influences inotropy?

A
  • AP plateau phase (excitation contraction coupling)
  • External ion gradient (NCX and Na/K ATP ase transporters)
  • Force frequency relationship
  • ANS
  • Drugs
    \ Caffiene, inhibits PDE prevents cAMP breakdown
    \ Digoxin, cardiac glycoside inhibits Na/K ATPase, NCX reverses
    \ Verapamil, Ca channel inhibitor
  • Heart failure
31
Q

How does chonrotropic state influence CO?

A
  • HR increases, CO increases
  • Force frequency relationship
  • High HR reduces SV, decreasing CO
32
Q

What does the equilibrium between CO and VR represent on the venous return/ CO curve?

A

This is the steady state equilibrium at which the heart works with some transient deviations.

The MRAP at this point = mean systemic filling pressure

33
Q

What are normal values for Ejection Fraction?

A 
Rest = ~50%
Exercise = ~85%
34
Q

What are the two types of ventricular function curves?

A

Stroke volume vs preload

Stroke Work vs preload

35
Q

Why is stroke volume vs preload not used?

A

Stroke volume is difficult to measure and not independent of afterload

36
Q

Why is stroke work vs preload good?

A

Not susceptible to changes in after load

LV EDP is used instead of EDV as it is easier to measure

If MAP increases, SV decreases keeping SW constant.

37
Q

What does a ventricular function curve represent?

A

Summery of the P-V and frank-starling relations

38
Q

A family of curves on the ventricular function curve represents?

A

Different inotropic states

39
Q

What cardiac factors does a ventricular function curve account for?

A

Preload
After load
Inotropic state

40
Q

Describe how LA pressure is obtained?

A

A fluid filled catheter with a ballon tip is passed through the femoral vein via the heart into the PA. Ballon inflates and measures the pre-capillary pressure which is representative of the LA pressure mostly…

This can measure both pulmonary artery pressure and pulmonary wedge pressure.

41
Q

Describe ventricular diastole:

A
  • Begins with closure of the semilunar valves
  • Followed by isovolumetric relaxation (ends when atrial pressure exceeds that in the ventricle)
  • AV valves open and rapid ventricular filling occurs
  • This is followed by a phase of slow filling (Diastasis)
  • Atrial systole terminates ventricular diastole and the cycle begins again
42
Q

Generically describe the phases of the cardiac cycle:

A

1) Passive ventricular filling (diastole)
2) Isovolumic contraction (systole)
3) Ejection (Systole)
4) Isovolumic relaxation (diastole)

43
Q

What can be used as a measure of preload?

A

EDP

44
Q

Whats important regarding the heart when it comes to afterload?

A

Fibre tension and chamber geometry (law of laplace)

45
Q

Describe the law of laplace:

A

Wall stress (tension, T) = P*r / 2 x wall thickness

46
Q

Regarding the law of laplace what happens with increased preload?

A
  • Increased preload = Inc. vol

= Decreased wall thickness
= Increased ventricular radius
= Increased wall tension to generate the same pressure

47
Q

Regardin the law of laplace what happens with increased afterload?

A

Increased pressure needed thus the wall stress needs to be produced.

48
Q

What does increased inotropy do to the PV loop?

A

Increases the max potential pressure that can be generated thus the steepness increases.

49
Q

Check lecture PV loops

A

Now and add to this

50
Q

Whats the implication of the frank starling mechanism with two sides of the heart:

A

System is closed

  • Both sides must pump same volume over time
  • Hence changes must effect both L and R
  • Increased afterload leads to increased preload

Arrhythmias impact balance

51
Q

Describe the the P-V relationship of the heart in response to increased afterload over one cardiac cycle;

A

Increased afterload in Aorta =

  • Decreased LV SV
  • The RV has continued pumping into pulmonary circuit, increased stretch of capacitence circuit increases pressure of flow into LV
  • LV EDV increases (preload)
  • SV increases

Refer to diagram if need be

note if EDV increases, the ventricle will not contract down to the same volume even if SV is increased

52
Q

How does dP/dT assess ventricular performance?

A

Max dP/dT used as indicator of contracility

*Negative during relaxation

53
Q

What is stroke work? and its formula

A

The work done by the heart to eject blood

SW = P x dV/dt

Estimated by MAPxSV

Stroke work is the area inside the PV loop, bottom wedge is the passive filling + Atrial contraction + inertia of ventricular filling (but is negligible)

Cardiovascular MBCHB2 (31 decks)

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