Cardiac Cycle Mechanical and Electrical Events - Heart Sounds and Performance

Question 1

What is the first heart sound?

Answer 1

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

Question 2

What is the second heart sound?

Answer 2

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

Question 3

What accounts for heart sound splitting?

Answer 3

corresponding left and right sided valves do not close exactly simultaneously

Question 4

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

Answer 4

yes

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

Question 5

When is RV stroke volume > LV stroke volume?

Answer 5

inspiration (opposite true during expiration)

Question 6

What is s3?

Answer 6

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)

Question 7

What is s4?

Answer 7

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)

Question 8

What is the cause of cardiac murmurs?

Answer 8

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

Question 9

3 types of murmurs

Answer 9

systolic, diastolic, continuous

Question 10

What are 3 causes of systolic murmurs?

Answer 10

outflow tract obstruction, AV valve regurgitation, interventricular communication

Question 11

What are 2 causes of diastolic murmurs?

Answer 11

semilunar valve regurgitation, AV valve obstruction

Question 12

3 paradigms for assessing cardiac performance

Answer 12

1. pumping performance
2. cardiac muscle performance
3. chamber function

Question 13

CO =

Answer 13

SV * HR

Question 14

What determines stroke volume?

Answer 14

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

Question 15

4 parameters that describe pumping performance

Answer 15

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

Question 16

3 parameters that describe cardiac muscle function

Answer 16

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

Question 17

5 parameters that describe ventricular chamber function

Answer 17

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

Question 18

The force available to distend myocardium at end diastole

Answer 18

preload –> underpinning of frank starling relationship

Question 19

What does preload determine?

Answer 19

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

Question 20

How is preload derived

Answer 20

from ventricular end diastolic pressure

Question 21

Is the degree of sarcomere shortening uniform throughout the ventricle?

Answer 21

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

Question 22

Why does increasing diastolic length require progressively greater force?

Answer 22

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

• places a ceiling on achievable ventricular end diastolic volume

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

What are some pathophysiologic consequences of increasing preload?

Answer 25

pulmonary hypertension, edema in large spaces like legs