Cardiac Cycle Mechanical and Electrical Events - Heart Sounds and Performance Flashcards Preview

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Flashcards in Cardiac Cycle Mechanical and Electrical Events - Heart Sounds and Performance Deck (25)
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1
Q

What is the first heart sound?

A

S1 –> caused by AV valve closure (two components: mitral and tricuspid)

2
Q

What is the second heart sound?

A

S2 –> caused by semilunar valve closure (two components: aortic and pulmonic)

3
Q

What accounts for heart sound splitting?

A

corresponding left and right sided valves do not close exactly simultaneously

4
Q

Does relationship of aortic and pulmonic valve closure vary with respiration?

A

yes

e.g.. inspiration augments systemic venous return –> increases RV stroke volume, prolongs RV ejection –> delays pulmonic valve closure

5
Q

When is RV stroke volume > LV stroke volume?

A

inspiration (opposite true during expiration)

6
Q

What is s3?

A

rapid early ventricular filling (not normally audible in adults) –> indicates accentuated early ventricular filling or disordered diastolic compliance

–> basically getting most of blood into ventricle fast so there is a rapid deceleration of the blood in the ventricle
(160 msec after S2)

7
Q

What is s4?

A

accentuated late diastolic filling due to atrial contraction –> indicates abnormal diastolic compliance and accentuated atrial contribution to ventricular filling

–>basically “passive” diastole isn’t working right so the atrial kick has to be stronger to compensate
(100msec before S1)

8
Q

What is the cause of cardiac murmurs?

A

turbulent flow due to abnormally increased flow velocity –> reynolds relationship: if flow velocity > turbulence threshold will get sound

9
Q

3 types of murmurs

A

systolic, diastolic, continuous

10
Q

What are 3 causes of systolic murmurs?

A

outflow tract obstruction, AV valve regurgitation, interventricular communication

11
Q

What are 2 causes of diastolic murmurs?

A

semilunar valve regurgitation, AV valve obstruction

12
Q

3 paradigms for assessing cardiac performance

A
  1. pumping performance
  2. cardiac muscle performance
  3. chamber function
13
Q

CO =

A

SV * HR

14
Q

What determines stroke volume?

A
  1. end diastolic volume - volume available to eject and determinant of available contractile force ( EDV is determined by LVEDP)
  2. force opposing ventricular ejection - resistance determines the contractile force required to shorten and eject and largely determined by great vessel pressure
15
Q

4 parameters that describe pumping performance

A

stroke volume, ventricular developed pressure, ventricular end diastolic pressure, arterial systolic pressure

16
Q

3 parameters that describe cardiac muscle function

A

end diastolic force, peak or end systolic force, systolic shortening fraction

17
Q

5 parameters that describe ventricular chamber function

A

end diastolic volume, end systolic volume, ejection fraction, end diastolic wall stress, systolic wall stress (peak and end)

18
Q

The force available to distend myocardium at end diastole

A

preload –> underpinning of frank starling relationship

19
Q

What does preload determine?

A

end diastolic sarcomere length –> length from which systolic shortening begins –> determines:

  1. ventricular volume at end diastole that is available for pumping
  2. the contractile force myocardium is ableto develop
20
Q

How is preload derived

A

from ventricular end diastolic pressure

21
Q

Is the degree of sarcomere shortening uniform throughout the ventricle?

A

no –> typically between 10 and 20% up to a maximum of 33%

22
Q

Why does increasing diastolic length require progressively greater force?

A

stiffness changes mostly due to titin –> slack at small lengths but taut at longer lengths

  • places a ceiling on achievable ventricular end diastolic volume
23
Q

Why does lengthening myocardial diastolic length increase systolic force that can be developed?

A

increasing cell length compresses sarcomeres laterally enhancing interaction between actin/myosin

24
Q

What is the difference between the diastolic force-length relationship and the end-systolic force-length relationship in myocardium?

A
  1. diastolic force-length relationship is non-linear–> myocardium is stiffer as it gets longer and requires more force increment
  2. systolic force-length relationship is reasonably linear –> as myocardium gets longer, it generates proportionately more force because of the geometric proximity of actin/myosin
25
Q

What are some pathophysiologic consequences of increasing preload?

A

pulmonary hypertension, edema in large spaces like legs

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