Cardiac Performance Flashcards

1
Q

What is the primary function of the heart?

A

To eject a sufficient amount of blood into the arterial system to maintain blood pressure that will assure adequate blood flow to all the peripheral tissues

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2
Q

How do you calculate stroke volume?

A

EDV-ESV

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3
Q

How do you calculate ejection fraction?

A

SV/EDV x 100

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4
Q

How do you calculate cardiac output?

A

SV x HR

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5
Q

How do you calculate Cardiac Index?

A

CO/SA

Where SA = body surface area

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6
Q

How do you calucalate Left Ventricular Stroke Work (LVSW)

A

SV x left ventricular pulse pressure

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7
Q

Do you need to be able to identify all the steps of heart contraction on a pressure volume loop?

A

Yes

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8
Q

The area inside the pressure/volume loop represents what?

A

The work done on that bolus of blood (LVSW)

It is literally SV x LVPP

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9
Q

How do you calculate the Left ventricular pulse pressure?

A

Systolic pressure- diastolic pressure

It’s a pulse pressure

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10
Q

What is the definition of preload?

A

Tension (stretch) in ventricular wall at end of diastole (proportional to EDV)

However, we can’t really measure that, so we use End Diastolic Volume in its place.

Preload= EDV

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11
Q

What determines resting fiber length?

A

Preload

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12
Q

As preload increases, what happens to stroke volume? Why?

A

Stroke volume increases due to the muscle being stretched to its optimal length and it ejects more blood

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13
Q

What law is this: the strength of the contraction of an isolated cardiac muscle fiber is a function of muscle fiber length (length-tension relationship)

A

Frank-Starling Law of the Heart

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14
Q

When venous return to the right heart increases, what happens to the output of the left heart?

A

It will also increase

Right and left ventricular outputs are thereby matched

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15
Q

With increased HR, what happens to ventricular filling time, and therefore, preload?

A

Ventricular filling time is reduced, so preload will be reduced.

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16
Q

With increased HR, ventricular fill time is reduced, and therefore preload is reduced. What effect does this have on Cardiac output in the ABSENCE of sympathetic stimulation?

A

Under 150bpm, CO is not affected since the decreased SV is compensated for by the increased HR.

Above 150bpm, CO decreases

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17
Q

Increased HR decreases ventricular filling time, and therefore decreases preload. How does this affect Cardaic Output in the PRESENCE of sympathetic stimulation?

A

Cardiac output can increase dramatically because SV is preserved due to increased contractility.
CO=SV x HR

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18
Q

What is this: the ability of ventricle to distend under pressure

A

Ventricular compliance

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19
Q

A highly compliant chamber will undergo a _____ change in volume with a small change in pressure

A

Large

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20
Q

In hypertrophy and ischemia, what happens to compliance?

A

Compliance is reduced

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21
Q

Low compliance has what effect on ventricular pressures and ventricular filling?

A

High ventricular pressures develop with just a small amount of volume added to the chamber

Filling is retarded (no offense intended with the use of that word)

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22
Q

What effect will decreasing intrathoracic pressure have on RV stroke volume?

A

Increased, which also increase LV preload

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23
Q

What effect does increased CVP (Central venous pressure) have on RV stroke volume?

A

Increased RV stroke volume= increased LV preload

24
Q

If you increase the pressure gradient between the inside and outside of the ventricle (delta P), what will happen to RV filling?

(You increase delta P by either increasing CVP or decreasing intrathoracis pressures ex: inspiration0

A

Increased RV stroke volume = increased LV preload

25
Q

Atrial systole (kick) has a ____ effect on EDV under normal circumstances?

26
Q

When does the atrial systole (kick) have a very important effect on preload?

A

When filling time is limited (ex: high heart rate)

27
Q

Under normal conditions, what is the job of the pericardium?

A

Prevent the LV from being overexpanded

Also maintains alignment with major vessels

28
Q

What happens to preload if the pericardium becomes Over filled with fluid?

A

The hydrostatic pressure on the external surface of the heart will reduce ventricular compliance which reduces EDV and SV (preload is decreased)

29
Q

What is a clinical example of the pericardium being filled with fluid?

A

Cardiac tamponade

30
Q

What is the definition of Afterload?

A

Resistance against which the ventricle contracts

(For example, in the LV, the major components are arterial pressure, peripheral vascular resistance, arterial wall compliance, mass of the column of blood in the aorta, and the viscosity of the blood)

31
Q

What measurement do we use to estimate afterload?

A

Mean arterial pressure

DP + 1/3 PP
PP in the aorta btw

32
Q

If you increase afterload, what happens to SV?

A

Decreased SV

33
Q

With increased afterload, the aortic valve opens (sooner/later) and closes (sooner/later)

A

Opens later

Closes sooner

Causes increased ESV (more blood left in the heart at the end of systole) and a reduced SV

34
Q

How does the heart compensate for increased afterload (which would normally cause increased ESV and decreased SV)

A

It is compensated for by the Frank starling mechanism. The Right heart doesn’t know that the LV is having trouble ejecting the blood into the aorta, so it will deliver a normal amount of blood to the LV, causing it to stretch, which allows the LV to generate more force. SV is restored to normal.

35
Q

What effect does aortic stenosis have on afterload

A

Increased afterload

36
Q

What effect does elevated arterial pressure (hypertension) have on afterload?

A

Increased afterload

37
Q

How does the heart compensate for increased afterload?

A

It fills more during diastole=more stretch=bigger force of contraction
frank starling mechanism

38
Q

What is the definition of contractility?

A

The ability of the heart to do work at any given fiber length

(Independent of preload and afterload)

39
Q

What types of factors affect contractility?

A

ANS acitivty (mainly SNS)

Circulating hormones (ie. epinephrine)

Catecholamins increase Ca+ influx and availability = more cross bridges=more force

40
Q

what is the primary contributor to afterload?

A

The pressure in the aorta

41
Q

What does the area in the loop in a pressure/volume loop represent?

A

Ventricular stroke work

42
Q

Why does the heart get bigger after a long period of hypertension?

A

To increase the frank starling method of compensation

-heart is bigger=larger volume of blood in ventricle=more forceful contraction

43
Q

How does norepinephrine affect contractility?

A

It stimulate B1 receptors, which increases contractility, and increases the SV at a given EDV. This is an increase in ejection fraction

postive inotropic effect

44
Q

With SNS stimulation, what happens to the length of systole?

A

It is shortened, so that time for diastole is not shorter, and the filling time is maintained

45
Q

What effect will increasing contractility have on ejection fraction and ESV?

A

Ejection fraction will increase

ESV will decrease (less blood in ventricle at end of systole)

46
Q

As contractility increases what is the effect on:
Ejection velocity

Stroke volume

ESV

A

Ejection velocity increases

Stroke volume increases

ESV decreases

TEST QUESTION*

47
Q

How do we estimate contractility?

A

By estimating the ejection fraction using ultrasound/echocardiogram.

48
Q

How do you calculate ejection fraction

A

SV/EDV x100

49
Q

What is a normal ejection fraction?

A

Normal 50-75%

50
Q

What is Treppe?

A

As HR increases, Ca++ accumulates, which increases contractility

Helps to maintain cardiac output at very fast HRs

51
Q

Is maximum HR a function of age or training?

52
Q

As exercise intensity increases, HR increases linearly. Does SV also increase linearly?

A

No, it is linear at low intensities, but *plateaus at about 40-60% of VO2 max

53
Q

Is the heart muscle aerobic or anaerobic?

A

Highly aerobic

54
Q

Does the efficiency of heart muscle increase or decrease with exercise

55
Q

What type of work increases during exercise: volume work (moving blood-preload) or pressure work (working against afterload)?

A

Volume work increases.

Volume work is energetically less costly than pressure work

56
Q

What is Left Ventricular Stroke Work?

How do you calculate it in a lab situation vs in the clinic?

A

It is the work done by the left ventricle in one stroke

LVSW= SV x LVPP
Only IF you have the values of the pressures in the left ventricle, which would be difficult to do in the clinic.

In the clinic, you would estimate LVPP with MAP

LVSW= SV x MAP

(MAP = diastolic Pressure + 1/3 pulse pressure)

57
Q

What is left ventricular minute work and how do you calculate it?

A

It is the amount of work done by the left ventricle in one minute

LVMW=LVSW x HR

BUT you might not always have the LVPP requreied to calculate LVSW, so you would estimate LVPP by using MAP

LVMW= SV x MAP x HR

(MAP= diastolic press + 1/3 Pulse pressure)
(LVSW= SV x LVPP)