The Cardiac Cycle 2: Heart Sounds and Perfomance

Question 0

What causes the first heart sound - S(1)?

Answer 0

AV valve (mitral and tricuspid) closure.

Question 1

2 broad causes of heart sounds?

Answer 1

Rapid acceleration /deceleration of blood flow (e.g. valve closing).
Turbulent (high velocity) blood flow.

Question 2

What causes the second heart sound - S(2)?

Answer 2

Closure of the semilunar valves.

Question 3

What effect does inspiration have on S(2)?

Answer 3

Inspiration -> increased systemic venous return -> prolonged RV ejection -> delay of pulmonic valve closure.
This delay can result in “splitting” of S2 into 2 sounds.

Question 4

What are S(3) and S(4)?

Answer 4

Both are from ventricular filling.
S(3): Early rapid ventricular filling. (hard to hear normally)
S(4): Late rapid ventricular filling from atrial contraction (very hard to hear).

Question 5

What produces heart murmurs, generally?

Answer 5

Turbulent flow due to abnormally high flow velocity.

recall Reynolds relationship

Question 6

Outflow tract obstructions (aka. stenosis), AV valve regurgitation, and interventricular communications would all produce what kind of murmur?

Answer 6

Systolic (ejection) murmur.

Question 7

AV valve obstruction and semilunar valve regurgitation would both produce what kind of murmur?

Answer 7

Diastolic (ventricular inflow) murmur.

Question 8

If you hear a systolic murmur with a split S(2), what’s one thing that could cause this?

Answer 8

Interventricular septum defect:
LV -> RV flow causes murmur.
Excessive RV filling delays pulmonic valve closure -> S(2) splitting.

Question 9

Stroke Volume * Heart Rate = ?

Answer 9

Cardiac Output

Question 10

2 broad factors determining stroke volume?

Answer 10

End diastolic volume.

Force opposing ventricular ejection.

Question 11

What are the two most important parameters affect ventricular performance?

Answer 11

Preload

Afterload

Question 12

What is “preload”?

Answer 12

The force available to distend the myocardium at the end of diastole.
(related to ventricular end diastolic pressure)

Question 13

What does the Frank-Starling Law of the Heart say?

Answer 13

The biggest factor affecting cardiac output is venous return.

Question 14

2 parameters preload affects?

Answer 14

Volume available for ejection.

Contractile force that myocardium can generate.

Question 15

What’s the theoretically maximum % shortening of cardiac sarcomeres?

Answer 15

30%

usually it’s more like 10-20%, though

Question 16

What accounts for cardiac myocytes’ DIASTOLIC force-length relationship? Linear or not?

Answer 16

Largely, titin.

Not linear.

Question 17

What accounts for cardiac myocyte’s END SYSTOLIC force-length relationship? Is it linear or not?

Answer 17

Sarcomere properties:
Inotropic state (i.e. [Ca++]).
Myosin-actin proximity.
Linear.

Question 18

What is the definition of ventricular preload? What measure correlates with it?

Answer 18

The distending force present in the ventricle available to fill its volume at end diastole.
Ventricular end diastolic pressure (LVEDP) is used to assess preload… but there’s more to it than that.

Question 19

What does preload meet for sarcomere shortening, contractile strength, stroke volume, and systemic arterial pressure?

Answer 19

More shortening.
Stronger contractions.
Greater stroke volume.
Greater systemic arterial pressure.

Question 20

Why is too much preload a bad thing?

Answer 20

Too much atrial pressure = edema, either systemic or pulmonary.

Question 21

What’s a normal LVEDP in mmHg? How would this change in left ventricular hypertrophy?

Answer 21

normal LVEDP: 10-12mmHg

In hypertrophy, it increases due to reduced ventricle compliance.

Question 22

Do all cardiac myocytes shorten the same amount?

Answer 22

Nope. Endocardial myocytes contract more - this creates the effect of the heart wall thickening during contraction.

Question 23

What is the definition of afterload?

Answer 23

The load that ventricular muscle must overcome during systole in order to eject.
(in the left ventricle, correlated with systemic arterial pressure, but again, that’s not the whole story)

Question 24

How does increasing afterload affect stroke volume?

Answer 24

Increasing afterload decreases stroke volume.

Question 25

What does LaPlace tell you about the force (i.e. tension) on/from the ventricle wall during contraction?

Answer 25

As the volume decreases during contraction, the ventricle doesn’t need to exert as much force to maintain the same pressure.

Question 26

What is inotropy?

Answer 26

Inotropy refers to the fact that cardiac myocytes can alter their contractile strength for a given length. (based on inputs from autonomics, heart rate, metabolic state, etc.)

Question 27

End diastolic volume (EDV) - end systolic volume (ESV) = ?

Answer 27

Stroke volume (SV)

Question 28

For each preload and afterload, it’s not just the pressure in the ventricle at end diastole/systole, it’s also…

Answer 28

the force-length relationship at that time.

Question 29

2 major determinants of (end stroke volume) ESV?

Answer 29

Afterload.

Inotropic state.

Question 30

If diastolic volume (aka preload) increases, what will happen to the degree to which the myocardium can shorten?

Answer 30

The myocardium will shorten more, and stroke volume will increase.

Question 31

If afterload increases, what will happen to the myocardium’s ability to shorten?

Answer 31

The myocardium will shorten less, decreasing stroke volume.

Question 32

What’s the formula for left ventricle ejection fraction?

Normal range?

Answer 32

LVEF = SV / EDV
Normal: 55-70%
(Bear in mind that LVEF depends heavily on both preload and afterload, so low LVEF alone isn’t enough to conclude that the heart has a contractile problem. - and normal LVEF isn’t enough to conclude that it doesn’t)