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101 Cardiovascular Physiology 1 Fall 2013 > CVT 101 Cardiac Hemodynamics > Flashcards

CVT 101 Cardiac Hemodynamics Flashcards

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1
Q

Define Depolarization:

A

ionic exchange with sodium and potassium.

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2
Q

Define Repolarization :

A

normal resting cell potential

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3
Q

Define P Wave :

A

atrial contraction

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4
Q

Define QRS :

A

ventricular contraction

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5
Q

Define T wave:

A

repolarization

If we do not have repolarization, there will be no mechanics or electrical.

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6
Q

Define Systole & Diastole :

A

Systole: contraction of the ventricles (left side of the heart mainly because it is our systemic pump but we also have a stroke volume and cardiac output on our right side.)

Diastole: relaxation of the heart.

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7
Q

When does systole end and diastole begin?

A

end of the T is the end of systole, beginning of diastole

When something ends, something begins.

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8
Q

What throws off our electrolytes and what does that have to do with our conduction system?

A

Electrolytes. If we have to much potassium or salt, we are interfering with our conduction system.

If a patient takes to many diuretics or to much of there medication it could cause arrhythmia’s, CHF.

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9
Q

Pressure curves for the LA and RA are:

A

identical but the mmHg scale will be different

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10
Q

The pressures in the LA and RA will depend on :

A
  1. chamber size, compliance
  2. presence of disease,
    valvular disease or cardiomyopathy
  3. ejection fraction

Chamber size and compliance of the left and right atrium.
(Compliance meaning is the chamber able to relax enough.)

If the myocardium (sarcomeres) of the right or left atrium dilate and stretch it causes fibroses and scars. They are not designed to stretch that far.
They become ineffective chambers and non compliant so the pressure goes up and the ejections fraction starts to decrease.

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11
Q

What events lead to myocardial contraction ?

A

a. Conduction which is depolarization and repolarization
b. at the cell level or ionic exchange
c. loading conditions, (HR, blood pressures, intracardiac pressures)
d. actin, myosin, sarcomeres

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12
Q

Normal RA pressure :

A

3-5 mmHg

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13
Q

Normal LA pressure :

A

9-15mmHg

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14
Q

Components for both the RA & LA :

  • a wave is the result of :
  • x Decent is early atrial relaxation:
  • c wave occurs during RA & LA filling :
  • x’ decent:
  • v wave occurs due to:
  • Y decent:
A
  • a wave: occurs after the P wave. The result of atrial contraction. The right and left atrium contracts and delivers an additional amount of blood to the right and left atrium so I have an increase in volume (only contributes about 10-15%)
  • x decent: relaxing and filling. Depolarization.
  • c wave: MV & TV move / bulge into the RA & LA due to changes in the dimensions . RA & LA are filling and relaxin
  • x’ decent: is late atrial relaxation
  • v wave: an increase in atrial pressure due to RA / LA filling where it reaches a peak and is higher than the RV/LV pressure , the TV/MV open leading to rapid passive filling.
  • Y decent: the TV / MV are open with the continuation of rapid passive filling to diastasis
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15
Q 
Atrial pressure tracing 
A wave 
X descent 
C wave 
X’ descent 
V wave 
Y descent
A

A wave: occurs after the P wave. The result of atrial contraction. a wave is active ventricular filling.
X descent: relaxing and filling. Depolarization.
C wave: slight bump in pressures because the annulous is moving
X’ descent: End of T wave. Atria continuous drop in pressure.
V wave: V for Volume- atria are being filled.
When they are at their fullest they create the V wave. When we have all of this volume in the R and L atrium, the valves open. Slightly delayed after the T wave.
Y descent: Rapid passive filling. The pressures start to fall because atria are delivering the stoke volume to the ventricle. Called diastase’s. When the mitral valve opens there is rapid passive filling. The Mitral valve starts to close due to diastasis from the decrease in pressure. There is still blood flow through the mitral valve then at the end of diastases there is an A kick. generates an A wave, done with diastole, and the mitral valve closes.

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16
Q

How much stroke volume is delivered by the A kick?

A

A kick delivers about 10-15% to the total stroke volume to the LV. It depends on size of the atrium.

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17
Q

How often is the left atrium and right atrium being filled and by what?

A

Left atrium is continuously being filled by the pulmonary veins
Right atrium is being filled with the IVC and SVC

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18
Q

Whats happening during IVCT?

A

all of the valves are closed. end of diastole, beginning of diastole.
IVCT happens just before systole.

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19
Q

What is happening at the cell membrane?

A

depolarization

You have stress in the walls going up because the walls have to overcome the pressure, ionic change at the cell level. Pressure in the LV starts to drop at the end of systole because the stroke volume is going out the AO. The the LV pressure is less than the LA pressure the valve closes.

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20
Q

What helps propagate and deliver a stroke volume?

A

Aortic root helps propagate our stroke volume. The tunica media takes the blunt force to help deliver the stroke volume.

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21
Q

ICVT is during:

A

depolarization

end of diastole beginning of systole

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22
Q

IVRT is during:

A

repolarization

end of systole beginning of diastole

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23
Q

What opens the AO and PV?

A

The pressures in the LV and RV

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24
Q

How long is IVCT and IVRT during the cardiac cycle?

A

IVRT and IVCT are about 0.4 milli seconds

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25
Q

4 stages of diastole

A
  1. IVRT
  2. rapid passive filling
  3. diastasis
  4. A kick
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26
Q

pulmonary wedge pressure:

A

9-15mmHg

same as the LA

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27
Q

what is the refractory period?

A

time when the ventricles repolarized

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28
Q

absolute means:

A

no stimuli can affect the ventricle.

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29
Q

normal pressure in the vena cava?

A

3-5 mmHg

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30
Q

what is the pressure in the LA?

A

9-15mmHg

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31
Q

PRESSURE TRACING IN THE CARDIAC CYCLE.

DURING IVCT
beginning of systole. Valves are closed. Depolarization.
Whats happening to the pressure in the LV?

next phase is:

LV and RV relax and fill. V wave. end of systole beginning of diastole.

A

it is increasing to open the AO.

peak systole. AO and PV open

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32
Q

What would cause a large a wave?

A

Stenosis. Anything that obstructs flow to the ventricles

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33
Q

What would cause an increased V wave?

A

Regurge

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34
Q

Enlarged a waves would occur in any condition Which increases resistance to RV / LV filling, examples to be :

A

stenosis, anything that would constrict flow to the ventricles.

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35
Q

The a wave would be absent in what arrhythmia ?

A

atrial fib

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36
Q

Enlarged v waves occur when in the cardiac cycle and would occur due to what ?

A

anything that is going to add more volume to the left atrium or right atrium.
tricuspid regurge, mitral regurge, shunt. If there is a hole in the inter atrial septum, if it is large it will add to the volume.

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37
Q

Is MS and TS a pressure or volume overload? What wave does it effect?

A

For MS and TS is a pressure overload to the RA and LA. It increases the a and v wave but primarily it effects the a wave.

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38
Q

In a normal pressure curve, the appearance of the RV/LV pressure curves are:

What is the difference between them?

A

identical

the only difference will be in the pressure scale

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39
Q

Normal values on the pressure curve
RV is:
LV is:

A

RV is 25/5 – 30/10,

LV is 120/0-130/10

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40
Q

Components for a Normal RV/LV Pressure Curves:

A
  1. a kick : due to the P wave , active RV/LV filling
  2. Isovolumic Contraction time : is from MV closure to AO valve opening , ventricles are full but not have contracted .
  3. Maximal ejection : PV/AV open , SV delivered reaching a peak pressure at peak systole.
  4. Minimal ejection occurs after peak ejection to the diacrotic notch ( PV/AV close)
  5. Isovolumic Relaxation Time occurs after the PV/AV close to MV/TV opening .
  6. Rapid Passive Filling : v wave
  7. Slow Passive Filling ( diastasis)
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41
Q

normal pressure for LV:

A

0-10mmHg diastole

125-129 mmHg systole

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42
Q

Coaptation:

A

when leaflets close or meet.

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43
Q

AO leaflets should be

A

thin and mobile.

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44
Q

NORMAL ARTERIAL PRESSURE CURVES AO/PA

PA/AO pressure curves are:

A

identical the difference being the pressure scale

Pressures may vary due to the RV/LV size & volume , EF% and presence of disease.

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45
Q

Normal values for the Arterial pressure curve
PA is:
AO is:

A

PA is 25/5 – 30/10

AO is 120/60-130/80

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46
Q

NORMAL ARTERIAL PRESSURE CURVES AO/PA

what is happening to the LV during IVRT?

A

It relaxes

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47
Q

Whats happening in the PA?

A

IVCT, pressure in the RV is going to increase. RV pressure has to be higher for the PA to open.

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48
Q

what is diastolic failure?

A

When the LV cant relax and fill

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49
Q

Components of Arterial Pressures AO & PA
A upstroke:
Diacrotic Limb:
Diastolic run off:

When does the AO and PV open?

A

A upstroke – anacrotic limb
Diacrotic Limb- a decrease in pressure at which time the AO/PA valves close
Diastolic run off systemically or to the capillary bed.

When does the AO and PV open? at the end of IVCT
We will have maximal ejection. End of diastole, beginning of systole, IVCT.

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50
Q

During AO/PA pressure tracing

DIacrotic notch or Diacrotic Limb
PA AO close
drop in pressure in the artery because we have a decrease in volume
end of diastole and beginning of systole the LV contracts and RV contracts
IVCT
AO and PA open
Maximal ejection
peak systolic pressure
minimal ejection
Pressure dropping
AO and PA close
Pressure just drops in the vessel throughout systole.
A 
DIacrotic notch or Diacrotic Limb
PA AO close
drop in pressure in the artery because we have a decrease in volume
end of diastole and beginning of systole the LV contracts and RV contracts
IVCT
AO and PA open
Maximal ejection
peak systolic pressure
minimal ejection
Pressure dropping
AO and PA close
Pressure just drops in the vessel throughout systole.
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51
Q

Things that effect AO and PA pressure curves are:

A
  1. The size of the chamber
  2. compliance of the myocardium
  3. RV end diastolic volume
  4. overall ejection fraction
  5. presence of disease
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52
Q

systolic motion of the aortic root is

A

when the cardiac output is being pushed out of the AO during systole.

53
Q

PA wedge is the pressure from what chamber ?

A

LA

normal pressure is 9-15mmHg

54
Q

RA normal pressure is:

A

is 3-5 normally

55
Q

What happens with AI?

A

The pressure gradient drops because the blood volume decreases in the AO because it is going back into the LV during diastole.
AO and PA close at the end of systole.
It has dropped down to 40mmHg instead of being 80mmHg

56
Q

IS AI or PI a Volume overload or a pressure overload?

A

Initially it is a volume overload.

Then it Increases LVEDP after

57
Q

In a stenosis or regurgitant blood flow, what type of flow do you not see?

A

When we look at a stenosis or a regurgitant blood flow, we are not looking at laminar blood flow. Causes LV walls to thicken initially and then dilate later causing LV failure.

58
Q

When does PI and AI occur?

What does it do to the LVEDP?

A

PI and AI occur during diastole.
so the LVEDP increases
Your LA pressure equals the LVED pressure.

59
Q

Mitral valve stenosis:

A

is a narrowing of the valve area

60
Q 
MS
Pathophysiology( changes in the MV leaflets )
A
  1. Increased leaflet thickness
  2. The commisures fuse
  3. Annular cacification
  4. Abnormal chordae
61
Q

MS

Pressure Alterations :

A
  1. diastolic gradient, increases pulmonary wedge pressure. increases left atrial pressures
  2. if we have an increased pressure in the LA 30-40mmHg, (PA pressure is 60mmHG) the pulmonary vascular bed will respond with resistance. That causes the right heart to have pulmonary hypertension.
  3. On our pressure curve, what wave is going to increase? the a wave and the a wave will increase
  4. Mitral regerge (incompetent valve)
    whats another leason.
62
Q

venous congestion:

A

the RA is already full

63
Q

MS

Incidence:

A

rare, more females than males

64
Q 
Mitral stenosis (MS) and Tricuspid stenosis (TS) 
Mitral Regurge(MR) and Tricuspid Regurge (TR)

Are these a volume overload or a pressure overload?

A 
Mitral stenosis (MS) and Tricuspid stenosis (TS) 
is pressure overload to the RA and LA.
Mitral Regurge(MR) and Tricuspid Regurge (TR) 
is a volume overload.
65
Q

In MS , what pressures are increased ?

Is this a distolic gradient ?

A

atrial pressure

yes because it during diastole

66
Q

In the pressure tracing with MS, what happens to the a wave ?

A

increases because the pressure goes up.

67
Q

Atrial fibrillation will cause a loss of what wave in the atrial tracing ?

A

a wave

68
Q

In MS what will decrease and increase?

A

In MS with an increase in stenosis there will be a decrease in the MVA and an increase in the gradient.

69
Q

What happens to the LV with MS?

A

It will be hyper-dynamic.

70
Q

Tricuspid Stenosis

•Similar findings in the right heart as in the left with MS.

A

also rare. The only difference is the pressure scale.

71
Q

What anatomical changes would we see with TS in the right heart?

A

RA will dilate

72
Q

What does TS do to the pressure in the RV ?

A

Increase HR to maintain stroke volume to the pulmonary valves.

73
Q

With TS, What wave on the Right atrial pressure curve would be increased ?

A

exact same as the MS so there will be an increase in the a wave.

diastolic murmur

74
Q

MR :

A

incompetent leaflets causing insufficiency during systole.

75
Q

Etiologies for MR :

A
  1. abnormal coaptation of anterior and posterior leaflets. can be due to abnormal cordae.
  2. cordal elongation
  3. abnormal annulous- dilated
  4. Mitral valve prolaps (cases regurge)
  5. mixomatis leaflets: abnormal change in the spongiousa layer like popcorn.
  6. flail of the mitral leaflet (can be anterior or posterior leaflet)
  7. ruptured cordae
76
Q

What wave does MR effect?

A

Increased v wave on the left atrial pressure curve

77
Q

If you have a normal valve that is leaking, what is causing that valve to leak?

A

You can have a normal valve but it cant stay shut so it leaks due to increased LVEDP. Once the problem is fixed mitral regurge is fixed.

78
Q

What chamber is MR going back into?

A

The LA is being filled by the pulmonary vein flow and the Mitral regurgitant volume

79
Q

What happens to the C.O / SV in a patient with significant Mitral regurgitation

A

Increased HR to try and get the SV

80
Q

TR

Tricuspid is a volume overload to the right heart , what changes will we see ?

A

occurs during systole. Increase RA and contractability.

81
Q

What happens to the RAP when there is TR ?

A

goes up

82
Q

TR

What happens to the RVSV ? What does the RV have to do to maintain that SV ?

A

SV goes down

To maintain stroke volume, the HR increases.

83
Q

Etiology for TR:

A

predominantly pulmonary hypertension, secondary: tricuspid valve prolapse, Chordal rupture,

84
Q

Etiology for AS:

A

narrowing of the aortic valve area

85
Q

Acquired AS:

A

a. acquired adult degenerative disease (natural aging process)
hypertrophic cardiomyopathy-obstructs the outflow track
b. rhumatic heart disease
c. disfuctioning aortic valve replacement, whether tissue or mechanical
d. bacterial endocarditis

86
Q

Congenital AS:

A

a. bicuspid aortic valve, unicuspid valve
b. congenital AS
c. hypertrophic
d. sub aortic membrane (it is congenital)

87
Q

What happens when our LV fails?

A

-When our LV fails, our AO will not open very much because it takes pressure to open the valve. The heart will increase the HR to compensate for that.

88
Q

How does AS impact the LV ?

A

Thickens the LV. AS causes ventricular remodeling.

89
Q

AS:

Is it a pressure overload to the ventricle ? And how would the ventricle respond ?

A

The LV has a pressure overload. The ventricle will be able to compensate for the pressure if it is healthy. If it is unhealthy it iwll not be able to produce the ejection fraction.

90
Q

Does AS produce a systolic or diastolic gradient ?

A

systolic gradient

91
Q

How is that reflected in the LV pressure Tracing ?

A

Generate a harder pressure to get the AO open. AO is about the size of the end of a pencil.

92
Q

What can accelerate AS and MS in the valves?

A

pressure gradient goes up. High blood pressure accelerates stenosis in the valves.

93
Q

Pressure alterations in AS:

A
  1. abnormal systolic gradient
  2. abnormal increase in our LVOT pressure and velocity because of the abnormal gradient
  3. When we look at the AO pressure curve it is delayed because of the AS
  4. Increase in LA pressure
  5. increase in LVEDP
  6. decrease in cardiac output and stroke volume
  7. the sequella cascade
94
Q

Can AS be repaired?

A

no, it has to be replaced.

95
Q

If you have a high LAP, where will it reflect?

A

back to your vascular bed, which increases pulmonary vascular resustance, increase in pressures RA

96
Q

What does the Ventricular Pressure wave reflect due to AS?

A

The pressure increases

97
Q

PS is similar to what other type of stenosis?

A

AS

98
Q

How does PS impact the RV? And pulmonary vascular bed?

A

It increases our systolic pressures

High pressures in the Pulmonary vascular bed and pulmonary vascular resistance

99
Q

Do we see the same changes on the right as we do on the left for AS?

A

yes

100
Q

What happens to the right heart pressures, RAP. RVEDP, can we have pulmonary hypertension?

A

Yes, the pressures go up in the RAP and RVEDP.
There will be pulmonary hypertension.
The left heart changes because it does not have the normal volume.
Decreased return to the left heart. EF is 30, pt wil be in CHF

101
Q

What can dilate with PS?

A

The AO root

102
Q

Subaortic stenosis: Is an abnormal narrowing of the LVOT due to the following etiologies:
Congenital/Genetic:
Aquired:
Subaortic Membrane:
Idiopathic Subaortic Hypertrophic Stenosis:

A

Congenital/Genetic: Born with hypertrophic cardiomyopathy which is very narrowed LVOT
Aquired:Hypertension, AS, LVOT obstruction because the walls are so thick it narrows the LVOT
Subaortic Membrane:Causing LVOT obstruction
Idiopathic Subaortic Hypertrophic Stenosis: Hypertrophic cardiomyopathy (IHSS)

103
Q

Sever LVH: systolic anterior motion of the mitral valve

A

Where the mitral valve is sucked into the outflow tract. We have an abnormal systolic pressure gradient in the LV

104
Q

SubPulmonic Stenosis is a narrowing of the RVOT/Infundibulum an obstruction to blood flow due to:

  1. Congenital Lesion:
    2: Acquired:
A
  1. Congenital Lesion:
    a. infundibular stenosis: obstruction to the outflow from the RVOT to the PA residual defect from a congenital defect
    — infundibular stenosis can be caused by:
    PA atresia
    no pulmonary artery
    PS
    2: Acquired:
    RVH because of pulmonary hypertension
    pulmonic stenosis
    left sided disease
    tricuspid stenosis
    pulmonary hypertension
105
Q

AI etiology:

A

incompetent aortic valve

106
Q

AI is caused by:

A
  1. Adult degenerative disease
  2. Rheumatic heart Disease (effects the commisures, AO may not close)
  3. Congenital; Bicuspid Aortic Valve, AS
  4. Aortic Root Disease (severely dilated)
  5. disfunctioning prosthetic valve, whether mechanical or tissue
  6. bacterial endocarditis
  7. aortic valve prolapse and torn cusp
  8. disection (is a tear in the tissue where your intima is seperated from the media.
107
Q

Aortic dissection:

A

It is a tear in the tissue, where your intima is seperated from the media

108
Q

Pressure alterations in AI:

What happens to the LVEDP due to AI?

A

Increase EDV
pressure in LV Increases
AO pressure decreases

109
Q

Pressure alterations in AI:.

What happens to the AO diastolic pressure?

A

It decreases

110
Q

Pressure alterations in AI:

How does the LV respond to AI?

A

Slight thickening of the LV
mild LVH
then the LV dilates over time

111
Q

Pressure alterations in AI:

Will AI be a volume or a pressure overload to the LV?

A

First will be a volume overload,
then progress to a pressure overload.
LVEDP will go up
Pressure in the LA will go up

112
Q

Pressure alterations in AI:

What is the normal pressure gradient?

A

between 60-80mmHg

113
Q

Can AS cause AI?

A

yes

114
Q

PI:

How does PI impact the RV?

A

Pressure goes up, volume goes up, walls thicken, increase the contractility, becomes hyperdynamic

115
Q

PI:

What happens to the pressures in the RV, RA and the venous system on the right?

A

RVEDP will increase. Pressure goes up in the RA causing pulmonary hypertension and TR causes IVC congestion causing swelling in the legs, tender liver, kidney congestion.

116
Q

PI:

What happens to the PASV?

A

In the RV, if healthy will increase HR to have increased SV.

If unhealthy RV, there will be a decreased SV

117
Q

PI:

What type of gradient is produced?

A

Will be less

118
Q

PI:

The pressure gradient would be determined by what parameters?

A

Volume and pressure in PA will be decreased

119
Q

What side of the heart is more suseptible to disease?

A

The left heart because it pumps systemically.

120
Q

Normal cardiac pressures:

RA

A

3-5mmHg

121
Q

Normal cardiac pressures:

RV:

A

25-30mmHg systolic

0-5mmHg diastolic

122
Q

Normal cardiac pressures:

PA:

A

25-30mmHg systolic

5-10mmHg diastolic

123
Q

Normal cardiac pressures:

LA:

A

9-15mmHg

124
Q

Normal cardiac pressures:

LV:

A

120mmHg systolic

0-10mmHg diastolic

125
Q

Normal cardiac pressures:

AO:

A

120-130mmHg systolic

60-80mmHg diastolic

126
Q

CVP-Swan Ganz Catheter:
Why is it given?
How is it floated?

A

they are given to patients that are having a hard time monitoring their blood pressure or HR. It is floated through the RA to the RV out the PA on the right side.

127
Q

How do we get a pressure on the left side of the heart with a swan ganz?

A

out through the LPA then inflate the balloon and wedge it to look at the left side throught the capillary bed.

128
Q

What does intracardiac pressures tell us about the patient?

A

It tells us if the patient has a good stroke volume, blood pressure

101 Cardiovascular Physiology 1 Fall 2013 (6 decks)

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