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Cardio Week 1 > Lecture 12: Cardiac cycle 2, Heart Sounds and Performance > Flashcards

Lecture 12: Cardiac cycle 2, Heart Sounds and Performance Flashcards

1
Q

What causes heart sounds?

A

Rapid acceleration (or deceleration) of blood
Valve closing and opening sounds
Ventricular filling sounds (gallops)

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2
Q

What is S1?

A

First heart sound

Caused by AV valve closure (mitral and tricuspid)

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3
Q

What is S2?

A

Caused by semilunar valve closure

Aortic and pulmonic

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4
Q

What is splitting?

A

When the corresponding right and left sided valves do not close exactly simultaneously
Relationship of aortic and pulmonic valve closure varies with respiration
-inspiration augments systemic venous return so increases RV stroke volume and prolongs RV ejection
-this delays pulmonic valve closure so you can hear splitting upon splitting

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5
Q

How do you hear splitting?

A

Upon inspiration, the pulm valve closes later than aortic valve because there is more venous return
When you hear splitting on expiration, that means there may be LBBB because aortic valve is closing later than pulm valve

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6
Q

What is S3?

A 
Rapid early ventricular filling
Low frequency
160ms after S2
NOT NORMAL unless in young adults
If heard, can indicated accentuated early ventricular filling or disordered diastolic compliance
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7
Q

What is the significance of hearing S3?

A

Problem with ventricular systole (3 syllables)
Can indicate accentuated early ventricular filling
Or disordered diastolic compliance
Means that there may be a volume overload

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8
Q

What is S4?

A

Accentuated late diastolic filling due to atrial contraction
Low frequency
100 ms before S1
Not normally heard

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9
Q

What is the significance of hearing S4?

A

Problem with ventricular diastole (4 syallables)
Can indicate abnormal diastolic compliance (so you need that extra atrial kick)
Indicative also of accentuated atrial contribution to ventricular filling

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10
Q

What causes murmurs?

A

Turbulent (high velocity) blood flow
Flow velocity > turbulence threshold predicted by Reynold
Relationship will produce murmurs
Normal blood flow in cardiac chambers and vessels is
Laminar and silent
Higher the velocity, the greater the frequency
Cardiac murmurs and vascular bruits

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11
Q

What is the significance of turbulent flow?

A

Occurs if flow velocity exceeds critical value predicted by Reynolds relationship
Turbulence creates vibrations that are perceived as sound

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12
Q

What are types of murmurs?

A
  1. Systolic

2. Diastolic

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13
Q

What are the characteristics of systolic murmurs?

A

Associated with ventricular ejection and can indicate

i. outflow tract obstruction
ii. AV valve regurgitation
iii. Interventricular communications
iv. Aortic valve stenosis (only here S1 because aortic valve is too stenotic)
v. Atrial septal defect
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14
Q

What are the characteristics of diastolic murmurs?

A

Associated with ventricular INFLOW and can indicate

i. Semilunar valve regurgitation
ii. AV valve obstruction
iii. aortic valve regurgitation
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15
Q

What are the principal parameters that define cardiac performance?

A
  1. Heart rate
  2. stroke volume
  3. systemic arterial pressure
  4. Left atrial pressure
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16
Q

What are the circulatory performance parameters?

A
  1. Cardiac output
  2. systemic arterial pressure
  3. Systemic and pulmonary venous pressure
    • needs to be adequate to achieve satisfactory diastolic filling of ventricles
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17
Q

What are the three paradigms for assessing cardiac performance?

A
  1. pumping performance (how the heart does in pumping blood around)
  2. cardiac muscle performance
  3. chamber function (the integration of all variables that characterize and influence cardiac performance)
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18
Q

What is the cardiac output?

A

SV x HR = CO

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19
Q

What determines stroke volume?

A
  1. end diastolic volume (preload)
    • volume available to eject
    • determinant of available contractile force
    • determined by ventricular end diastolic pressure
  2. force opposing ventricular ejection (afterload
    • resistance to ejection that must be overcome to eject
    • determines the contractile force required to shorten and eject
    • determined by great vessel pressure
  3. contractility
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20
Q

What is the significance of preload and afterload?

A

The two most important operating parameters that affect ventricular performance

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21
Q

What is preload?

A

The force available to distend myocardium at end diastole
Determines end diastolic sarcomere length
Derived from ventricular diastolic pressure
The underpinning of the Frank-Starling relationship

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22
Q

What is the effect of preload on cardiac muscle shortening?

A

At constant aortic pressure and heart rate the work of the heart is capable of being varied within wide limits by variations in venous pressure
The most direct factor influencing the quantity of blood sent out from the ventricle is the intraventricular pressuWhat are the two parameters that preload affects to determine cardiac pumping performance?re by which the ventricle is distended during diastole

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23
Q

What is the effect of venous pressure on cardiac output?

A

The higher the venous pressure of blood (or return), the higher the output of blood (CO)
That’s how RV and LV are regulated to pump same amount

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24
Q

What is the effect of preload on intrinsic cardiac muscle contractile performance?

A

Dependence of peak isovolumic pressure on ventricular volume

More volume = more pressure = greater cardiac output

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25
Q

What are the two parameters that preload affects to determine cardiac pumping performance?

A
  1. ventricular volume at end diastole that is available to be ejected
  2. the contractile force that myocardium is able to develop
    The greater the volume, the greater the force (regardless of compliance)
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26
Q

What determines level of ventricular contraction and ejection?

A

The extent of systolic myocardial shortening

27
Q

What is the maximum sarcomere %shortening?

A

33% shorter = max shortening

Most circumstances it is 10-20%

28
Q

What is the relationship between stretching and contractile force?

A

As the ventricle is being stretched, the contractile force increases EXPONENTIALLY
Therefore, we can state that increasing myocardial diastolic length increases the systolic force it can develop

29
Q

What is the mechanism that leads to increased systolic force upon increasing diastolic length?

A

Increasing myocyte cell length compresses sarcomeres laterally (the lines get closer together), thereby enhancing interaction between actin and myosin filaments
That’s how preload increases available contractile force

30
Q

What are the two performance properties of myocardium?

A
  1. diastolic force-length relationship

2. end-systolic force-length relationship

31
Q

What determines diastolic force-length relationship?

A

Determined by nooncontractile components of the sarcomere like TITIN
Not linear but rather exponential and maintains length between 1.65 and 2.2 micrometers
Diastolic myocardium is not perfectly elastic so (change in force does not equal change in length)
As myocardium is stretched during diastole, it becomes stiffer to oppose overstretching of the ventricle

32
Q

What determines end-systolic force-length relationship

A

Determined predominantly by the contractile elements, such as myofilament proximity and inotropic state
Reasonably linear over the operating range of sarcomeres (so as cardiac muscle shortens, the amount of force it develops decreases…so longer lengths = more force)
Thus it is the recruitment of these sarcomeres that is exponential, not necessarily the contraction of them

33
Q

What would be the pathophysiologic consequences of increasing preload to meet demand?

A

If you crank up preload, you crank up pressure in atria
If you crank up pressure in atria, you get pulmonary and
Peripheral edema

34
Q

Why does preload matter?

A

Preload determines the end diastolic muscle cell length from which systolic shortening begins
Greater preload = greater force generation
Greater preload = more SV and increased systolic pressure

35
Q

What are the three stages of diastole?

A
  1. early rapid filling (fast velocity)
  2. slow mid-diastolic filling
  3. atrial transport filling (fast velocity)
    Slide 41 and 42 (the velocity shit)
36
Q

How does preload relate to end diastolic pressure?

A

Degree of myocardial stretch during diastole is determined by interaction of diastolic pressure and chamber compliance characteristics

37
Q

What is chamber compliance determined by?

A

Chamber architecture and myocardial properties

38
Q

Why is ventricular contraction complex?

A

Endocardium moves inward but epicardial surface does not move appreciably
3 layers of muscles
Subendocardial myoctes shorten the most (so some myocytes are shortening more than others)

39
Q

What are the key characteristics of ventricular afterload?

A

The load that ventricular muscle must overcome during systole in order to eject
The force that opposes the shortening during systole
From pumping perspective, it is the ventricular systolic pressure (or the pressure that opposes the ventricular contraction)

40
Q

What is the significance of afterload?

A

The greater the afterload, the greater the force needed to contract the ventricle

41
Q

What is the interaction among ventricular geometry, pressure and wall force?

A

As a container gets bigger, it increases interior surface area
As interior surface area gets bigger, there is more pressure pushing against it, thus making it easier to distend (stretching a balloon to make it easier to blow up)
Force = Pressure & CSA (cross sectional area)

42
Q

When is wall stress greatest?

A

Systolic wall stress is greatest at the onset of ejection as ventricular dimension is at its largest at that time

43
Q

What happens to wall tension (force) during systole?

A

It decreases

Even pressure increases, radius decreases at a faster rate so that’s why there is a net wall tension decrease

44
Q

What is the effect of decreasing LV volume on ventricular wall stress during course of systole?

A

Decrease in volume = decrease in wall stress

45
Q

What is the difference between the first half and second half of systole?

A

In the first half of systole, ejection LV pressure increases
In the second half, wall stress declines because of the large effect of the decrease in LV dimension
So during ejection, LV unloads itself and further facilitates muscle shortenings

46
Q

What is inotropy?

A

The property of cardiac muscle to alter its intrinsic contractile force
Cardiac muscle, unlike skeletal muscle has the ability to alter its contractile force primarily independent of its length
Increasing inotropy = increasing amount of force generated at any given sarcomere length

47
Q

What are the factors that regulate the myocardium’s inotropic state (contractility)?

A
  1. heart rate
  2. autonomic inputs
  3. myocardial metabolic state (oxidative and ionic)
48
Q

What determines EDV (end diastolic volume)?

A

Preload as characterized by end diastolic pressure and the diastolic force-length relationship

49
Q

What determines ventricular stroke volume?

A

SV = EDV – ESV

50
Q

What determines ESV (end systolic volume)?

A

Afterload as characterized by systolic pressure and end systolic force length relationship
As well as
Inotropic state that shifts the end systolic force-length relationship

51
Q

What is the significance of the Ventricular pressure-volume loop?

A

Allows one to assess cardiac pumping performance through P and V
Also allows one to predict what would happen if an insult were to occur
For instance, if you increase diastolic filling, ventricular volume will increase to allow for greater systolic force to eject greater SV
Increasing arterial pressure will limit the extent to which LV can eject

52
Q

Why is there a decrease in LV force in the middle of systole?

A

Because the radius (R value in LaPlace) decreases faster than the pressure (P value in LaPlace) increases, thereby decreasing force felt

53
Q

What happens if load is kept constant and end diastolic volume is increased?

A

Stroke volume will increase

54
Q

What will increasing the afterload accomplish?

A

Reduce systolic ejection and therefore decrease stroke volume
Determined by
i. arterial pressure
ii. Ventricular dimension

55
Q

What is the relationship between preload and SV?

A

Increased preload = increased SV

There is an upper limit of allowable LV filling pressures however so there is a limited range

56
Q

What is the relationship between inotropic state and SV?

A

Increased inotropic state = increased SV

57
Q

What is the relationship between afterload and SV?

A

If arterial pressure increases, afterload increases and the degree to which myocardium can shorten from a given EDV decreases…thereby decreasing SV
If EDV is constant and arterial pressure is decreased, SV will increase

58
Q

How can the body increase SV?

A
  1. increasing preload
  2. reducing afterload
  3. increasing the inotropic state
59
Q

Are the preload, afterload and inotropic adjustments acute or chronic adjustments?

A

Acute

Chronic adaptation = chronic remodeling of the geometry of the left ventricle…

60
Q

What is Left Ventricular Ejection Fraction (LVEF)?

A

A commonly used easily measured index of left ventricular contractile function
LVEF = (EDV – ESV)/EDV = SV/EDV
Normal: 55-70%
This is NOT a fixed number
Depends on preload, afterload and inotropy

61
Q

What are different factors that can affect EF (LVEF)?

A
  1. Increasing preload = increased EF
  2. Increasing afterload = decreased EF
  3. Increasing inotropic state = increase EF
62
Q

What is afterload determined by?

A

d is determined by arterial vascular resistance, cardiac output and ventricular diastolic and systolic dimension

63
Q

What is preload determined by?

A

Preload is determined by atrial pressure and ventricular diastolic dimension

64
Q

What is inotropy determined by?

A

Inotropy is determined by HR, autonomic regulation and metabolism

Cardio Week 1 (11 decks)

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