Echocardiography II - Part 2. Flashcards

1
Q

The velocity of the image is being recorded at 0.6 m/s. (1) By what technique could you use to establish a VTI and (2) what does the VTI mean?

A

(1) Trace the flow profile provides the velocity time intergral (VTI)/Flow velocity integral (FVI). This could be done manually or by the machine.

(2) VTI/FVI measures the mean velocity throughout the flow period. The peak velocity is automatically calculate within the flow trace.

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2
Q

What information does the flow velocity integral (FVI)/velocity time intergral (VTI) provide?

A

Flow integral is calculated by tracing the flow profile. Once the entire flow profile is traced, the VTI is displayed on the monitor in cm. The area under the flow velocity curve represents the distance a volume of blood travels.

As the VTI is directly proportional to the stroke volume, this information together with the area of a vessel or the valve of blood is flowing through can calculate the stroke volume

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3
Q

What primary vessels can systolic time intervals be measured from?

A

Aortic (LVOT) and pulmonary (RVOT) flow profiles.

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4
Q

What is the acceleration time (AT) of a flow profile?

A

(AT) is the time to peak flow measured from the onset of flow to the point of maximal velocity. This is typically measured at the baseline.

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5
Q

What is the ejection time (ET) of a flow profile?

A

(ET) is the time measured from the onset of flow to the end of flow at the baseline.

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6
Q

Obtaining the AT from the RVOT and LVOT [RVAT and LVAT, respectively] may be divided by the ET. What information does this provide?

A

These two systolic time periods are then divided to yield a variable that indicates what fraction of time is spent in reaching maximal velocity (AT/ET).

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7
Q

When would you measure the pre-ejection period (PEP)?

A

(PEP) is measured from the onset of the QRS complex to the onset of the systolic flow.

Here continuous wave aortic flow is used to measure ejection time (LVET) from the onset of flow to the end of flow at the baseline and pre-ejection period (PEP) from the start of the QRS complex to the beginning of aortic flow. A ratio, LVPEP/ET, is then calculated.

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8
Q

Define the isovolumetric relaxation time (IVRT) period.

A

The time interval from cessation of aortic flow to the beginning of transmitral flow

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9
Q

Where would you optimally measure the IVRT?

A

The isovolumic relaxation time (IVRT) is measured by placing a CW or PW signal in the left ventricular outflow tract on apical four or five chamber imaging planes near the mitral valve and recording part of both the aortic flow profile and the transmitral flow profile.

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10
Q

Describe the typical appearance of aortic flow profiles.

A

Aortic flow profiles are negative and have rapid acceleration compared to the slower deceleration rate.

Therefore, this gives the normal aortic flow profile an asymmetric appearance

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11
Q

What factors may affect peak aortic velocity?

A

Factors that may increase aortic peak velocity:
1. Sympathetic stimulation
2. High left ventriuclar preload
3. low heart rate
4. low blood viscosity
5. Certain drugs (e.g., inotropes, arterial vasodilators)
6. Noise stimuli as stress factors.

Factors that may decrease aortic peak velocity:
1. Negative inotropes (e.g., administration of β‐blockers)
2. Systolic dysfunction
3. Tachyarrhythmias
4. Dehydration

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12
Q

Measurement of the aortic flow is particularly relevant in some breeds predisposed to aortic stenosis, like the Boxer. What is a generally accepted normal value for peak aortic velocities? what is generally considered abnormal? what is considered equivocal? What about a Boxer with with a measured aortic velocity of 2.56 m/s?

A

Most normal healthy dogs have aortic flow velocities less than 2 m/s.
There is agreement that flows above 2.5 m/s are abnormal
Flows within the 2 to 2.5 m/s range are equivocal.

Aortic peak velocity values of up to 2.56 m/s are measured in Boxers in the absence of any evidence of discrete lesions in the LVOT by both transoesophageal and transthoracic echocardiography. Boxers may also have smaller LVOT areas compared with other breeds.

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13
Q

Describe the typical appearance of pulmonic flow profiles.

A

Pulmonary artery flow profiles are negative in all the views that can be obtained in small animals

The normal pulmonary flow profile has a very symmetrical shape with similar acceleration and deceleration rates.

Often it displays a rounded peak as opposed to the pointed peak velocity of aortic flow.

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14
Q

What factors may affect pulmonary flow velocity?

A
  1. Respiration affects flow within the right side of the heart. Therefore, increased venous return with inspiration increases pulmonary flow during inspiration.
  2. Heart rate. Fast heart rates in the dogs increase velocities.
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15
Q

What is a generally accepted normal value for peak pulmonary velocities?

A

Peak pulmonary flow velocity in the dog is typically less than 1.3 m/s in many studies. \

Normal pulmonic flow has lower velocity than aortic flow because of lower resistance within the pulmonary vascular system.

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16
Q

What is a generally accepted AT/ET (acceleration time to total ejection time) for pulmonary velocities? When is peak velocity typically reached during ejection period?

A

Pulmonary flow has a slightly longer ejection time and a reduced pre-ejection period compared to aortic flow because of the reduced afterload.

  1. AT/ET = 0.43
  2. Halfway
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17
Q

Describe the different types of pulmonary flow patterns which may be observed that can raise suspicion for pulmonary hypertension?

A

(A) Dome-like pulmonary artery (PA) flow in a normal dog.
(B) Sharp peak appearance of pulmonary artery flow in a dog with increased systolic PA pressure.
(C) Notched pulmonary artery flow in a dog with severely increased systolic PA pressure.

In dogs with pulmonary hypertension (B and C) there is a short flow acceleration time causing the pulmonary artery flow to resemble an aortic flow pattern as the peak velocity is reached sooner and the flow becomes asymmetric. The notch in the flow in image C is caused by flow reversal during the deceleration phase.

Systolic notching and an abnormally low AT/ET of less than 0.30 are some of the criteria evaluated to diagnose probability of pulmonary hypertension.

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18
Q

What is a more accurate indicator of left ventricular function, that factors out the effects of heart rate?

A

The pre-ejection time period (PEP) is very similar to the isovolumic contraction period where both the aortic and mitral valves are closed, and the ventricle is building up enough pressure to open the aortic valve.

A ratio of PEP to LVET is usually calculated to reduce the effects of heart rate on LVET. This is considered a more accurate indicator of left ventricular function. Reference ranges might vary slightly with breeds, however a ratio of less than 0.45 is usually considered normal.

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19
Q

When heart rates are variable, how do we measure systolic time intervals.

A

Time intervals measured from the longest cardiac cycles tend to be the most accurate indicators of left ventricular function when heart rates are variable. Avoid measuring during ventricular or supraventricular premature complexes or the beats that follow them.

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20
Q

Describe the typical appearance of transmitral flow profiles.

A

Transmitral valve flow profiles in all planes are positive, and when heart rates are slow enough, the two phases of left ventricular filling are well separated.

Once heart rates exceed approximately 125 beats per minute (bpm), the two phases begin to overlap and rates greater than 200 bpm show no separation of filling phases.

The E peak (rapid ventricular filling) should have a higher velocity than the A peak in the normal heart. The E:A ratio is greater than one in the normal canine heart, but both slow heart rates and high heart rates can decrease this.

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21
Q

What factors tend to affect transmitral flow?

A

Transmitral flow is affected by preload, myocardial relaxation, and heart rate.

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22
Q

How does slow heart rates affect transmitral flow?

A

Slow heart rates have increased A flow velocity due to increased volume associated with the atrial contraction, minimising the difference in E and A velocities.

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23
Q

How does high heart rates affect transmitral flow?

A

Rapid heart rates decrease the E velocity secondary to decreased early ventricular filling volume and increased flow associated with the atrial contraction.

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24
Q

What is MV Deceleration time (MV DecT)?

A

Deceleration time after rapid ventricular filling is the time from the point of maximal E velocity along its deceleration slope to the baseline (from the E wave the slope of the E wave is traced to the baseline). Calculations are automatically performed by the machine tracing the slope.

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25
Q

What factors influence the peak filling rate and MV flow deceleration in ventricular diastole?

A
  1. Isovolumic relaxation –> affects EARLY diastolic ventricular filling.
  2. Pressure gradient from LA to LV
  3. Ventricular compliance –> affects LATE diastolic ventricular filling.
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26
Q

What are some factors that INCREASE E-wave velocities?

A
  1. Increased LA pressure
  2. Decreased LV pressure secondary to increased rate of relaxation
  3. Decreased LV compliance
  4. Small MV Area
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27
Q

What are some factors that DECREASE E-wave velocities?

A
  1. Low LA pressure
  2. Decreased rate of relaxation
  3. Increased LV compliance.
  4. Large MV area
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28
Q

What are some changes observed in older dogs, with regards to MV flow profiles?

A
  1. E wave velocity decreases and A wave velocity increases
  2. E:A ratio decreases as a result
  3. E deceleration time increases –> influenced by body weight and heart rate
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29
Q

What is a large factor affecting E:A wave when assess transtricuspid flow velocities.

A

Respiration.

Peak tricuspid E wave velocity varies with respiration. Inspiration increases peak flow velocity while expiration decreases E flow velocities. The E:A ratio therefore increases with inspiration and decreases with expiration. The ratio can even be less than one under appropriate conditions in a normal heart.

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30
Q

Describe the flow profile with pulmonary venous flow (PVF)?

A

Pulmonary venous flow is continuous and phasic into the left atrial chamber.

Left atrial filling occurs predominantly during ventricular systole when the mitral valve is closed. The velocity of this systolic flow is directly related to mean left atrial pressure. During ventricular diastole when the mitral valve is open, blood flow into the left atrium is directly related to flow moving into the left ventricle and occurs at the same time as early transmitral valve flow (E wave). During atrial contraction there is reverse flow into the pulmonary veins called atrial reverse (Ar).

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31
Q

Atrial reverse occurs during the atrial contraction (A-wave) phase of diastole. What factors may affect atrial reverse?

A
  1. End-Diastolic LA pressure.
  2. LA function
  3. LV compliance
  4. Heart rate and rhythm.
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32
Q

How does Atrial Reverse correlate with ventricular filling pressures and compliance?

A

The ratio of transMVA wave duration to pulmonary vein Ar duration is correlated to left ventricular filling pressure and ventricular compliance.

A:Ar > 1, with normal diastolic function

33
Q

NO QUESTION: The following is a graph of LV diastolic function in cats.

A

And again..

34
Q

When assessing PVF, what are the differences in factors in cats and dogs affecting the flow profiles?

A

Cats:
Heart rate. Directly proportional to S-wave velocity
Age. Directly proportional to S-wave velocity AND Ar Duration.

Dogs:
Age. Ar velocity is DIRECTLY proportional whereas Ar duration is INVERSELY proportional.
Heart Rate. Directly proportional to S- and Ar velocity
Body weight. Directly proportional to Ar Duration.

35
Q

What is IVRT an indirect measurement of?

A

Ventricular relaxation

Delayed relaxation is reflected in longer IVRT. However, as atrial pressure increases this parameter “normalizes” again becoming less useful to assess relaxation. It is also affected by increased systolic aortic pressure and decreased left atrial pressure, both of which will prolong the IVRT and not truly reflect impaired relaxation.

36
Q

What are the typical pressures (Emptying and filling) of the left auricle observed in cats?

A

Feline auricular emptying velocity ranges from 0.19 to 1.0 m/s and filling velocity ranges from 0.24 to 0.93 m/s. There is a very weak correlation between left auricular flow and left atrial area or diameter in cats.

37
Q

What does a LAA flow velocity of (<0.25 m/s) typically indicate.

A

Stasis of blood flow is associated with lower than normal auricular flow and predisposition toward thrombus formation. At these pressure, the patient is at increased risk of spontaneous echocardiographic contrast and possible thromboembolism.

38
Q

What factors of systolic function is the heart dependent on?

A
  1. Preload: The force stretching the myocardium.
  2. Afterload: The force against which the heart must contract.
  3. Contractility: Dependent upon mechanisms within the myocardial cell. These involve the contractile proteins (actin and myosin), transport mechanisms for calcium, and regulatory proteins (troponin and tropomyosin).
  4. Distensibility
    5.Coordinated contraction
  5. Heart rate.
39
Q

What factors of systolic dysfunction is the heart characterized by?

A
  1. impaired pumping
  2. reduced ejection fraction
40
Q

How does PRELOAD affect systolic function?

A

It is dependent upon the amount of blood distending the ventricles at end-diastole.
Starling’s Law states that the greater the stretch, the greater the force of contraction. Increases in left ventricular diastolic volume, all other factors remaining constant, would therefore increase ventricular systolic function.

41
Q

How does AFTERLOAD affect systolic function?

A

Normally the heart will hypertrophy in response to increases in preload in order to normalize wall stress. The relationship of wall thickness to chamber size determines wall stress. The type of hypertrophy pattern seen in response to increased preload is eccentric, in that wall thickness and overall left ventricular mass increases in response to the increase in volume. In the absence of hypertrophy, afterload is increased within the volume overloaded left ventricle.

The peripheral pressure that the left ventricle must pump against is also afterload. Increased systemic or pulmonary pressure, vasoconstriction, and obstruction to ventricular outflow will also elevate afterload in the left or right side of the heart.

The compensatory hypertrophy pattern seen with increased afterload is concentric, where wall thicknesses increase with no increase in volume, and if the afterload is severe and chronic, hypertrophy may be at the expense of chamber size. Increases in afterload, without adequate compensatory hypertrophy, decrease the ability of the heart to contract effectively when all other factors are kept constant.

42
Q

How does CONTRACTILITY affect systolic function?

A

Cardiac output can be calculated by multiplying heart rate and stroke volume (CO = HR X SV)

Increases in heart rate with no other changes will result in greater cardiac output. Generally the body regulates heart rate to meet the metabolic demands of its tissues. Very high heart rates, however, can be detrimental to the heart itself and induce myocardial failure.

43
Q

How does optimal right ventricular function directly affect the right atrium?

A

Optimal right ventricular function allows the right atrium to (1) maintain a low pressure for adequate venous returnand to provide (2) low-pressure perfusion of the pulmonary vasculature.

44
Q

Describe the right ventricular function.

A

Contraction starts at the apex and moves towards the thin-wallls and complaint upper regions of the right ventricular chamber, resulting in slow continuous movement of blood through the RVOT/MPA and into the lung.

Right ventricular pressure remains LOW throughout systole as a result.

Isovolumetric relaxation and contraction are SHORTER and ejection is LONGER, than the left ventricle and continues even after the pressure continues to the decline.

45
Q

What happens when the RV undergoes increased afterload, acutely?

A

Acutely increased afterload results in dilation in order to maintain forward flow. Increased afterload also increases isovolumic contraction and ejection times. Chronic increases in pulmonary vascular pressure result in adaptive hypertrophy.

46
Q

As RV pressures increase during a pathological process, such as pulmonary hypertension, what happens to the left side of the heart?

A

Elevated right ventricular filling pressure under either condition causes a leftward shift in the interventricular septum affecting left ventricular function. The decrease in pulmonary flow decreases left ventricular preload and function. Therefore, dogs with pulmonary hypertension often show underloading of the left chambers.

47
Q

What are the M-mode systolic intervals (STI)?

A
  1. Left ventricular ejection time (LVET)
  2. Left ventricular pre-ejection period (PEP)
  3. Left ventricular PEP:ET
  4. Velocity of circumferential shortening (VCF)

REMEMBER: STI are indicators of FUNCTION not contractility. They are affected by preload, afterload, and contractility.

48
Q

What happens to PEP when afterload of the LV is increased (e.g., systemic hypertension, hypertrophic cardiomyopathy, ventricular outflow tract obstructions)?

A

When afterload is increased, the heart’s workload is increased, and as a result, the TIMEit takes to generate enough pressure within the left ventricle before the aortic valve can open is LONGER. Therefore, increased PEP

49
Q

What happens to VCF when afterload of the LV is increased (e.g., systemic hypertension, hypertrophic cardiomyopathy, ventricular outflow tract obstructions)?

A

The rate at which the heart can contract in the face of high afterload is also reduced, which results in reduced VCF.

50
Q

What happens to PEP and VCF when afterload of the LV is decreased?

A

Decreases in afterload allow the left ventricle to function with greater ease, and the force necessary to open the aortic valve is reached sooner resulting in decreased PEP.

The rate at which the heart can contract is also faster when the workload is reduced and VCF is increased.

51
Q

What happens to PEP and VCF when preload of the LV is increased?

A

High preload or volume within the left ventricle allows the Frank Starling mechanism as fibres are stretched and function is enhanced. This shortens PEP and increases LVET.

52
Q

What happens to PEP and VCF when preload of the LV is decreased?

A

Decreased preload does not allow enough force to be generated by fivers that are not at optimum length, and PEP is increased. Volume within the left ventricle affects LVET and so a reduction in volume and force of contraction will decrease LVET.

53
Q

What are the effects of preload, afterload and HR on systolic time intervals

A
54
Q

What are the effects of various cardiac diseases on systolic time intervals

A
55
Q

**Pre-ejection period (PEP) increases with which of the following? Select all that apply.

  1. Dilated cardiomyopathy
  2. Aortic stenosis
  3. Mitral insufficiency
  4. Ventricular septal defect
  5. Right heart failure.
A
  1. Dilated cardiomyopathy
  2. Mitral insufficiency
  3. Ventricular septal defect
  4. Right heart failure.
56
Q

How can you obtain stroke volume during a routine echocardiogram examination, without the machine giving you the values?

A

VTI is directly proportional to stroke volume. VTI is multiplied by the area of the vessel, valve, or orifice, through which flow volume is being calculated to obtain the stroke volume through that path in the heart.

This measurement can be done at any of the four valves. Flow velocity integrals at the mitral valve should use profiles that maximize peak E and A velocities.

Increases in FVI may suggest increased volume (as in a shunt).
Decreases in FVI can represent poor flow.

57
Q

Define the Tei/mpi Index.

A

The TEI or myocardial performance index (MPI) is an index of global myocardial function and includes both diastolic and systolic time intervals.

This measurement uses ventricular ejection time and the isovolumic periods (contraction IVCT and relaxation IVRT) to derive an overall assessment of global ventricular function. MPI (Tei Index) assesses global ventricular function using PW Doppler or TDI.

LV MPI = (IVRT + IVCT) / LVET = MCO - LVET / LVET

RV MPI = (IVRT + IVCT) / RVET = TCO - RVET / RVET

Where LV is left ventricle, RV is right ventricle, IVRT is isovolumic relaxation time, IVCT is isovolumic contraction time, MCO is mitral valve closing to opening time, TCO is tricuspid valve closure to opening time, and LVET and RVET are left and right ventricular ejection times, respectively.

58
Q

Describe how TEI/MPI index can be used using tissue Doppler evaluation.

A

Myocardial performance index can also be calculated using tissue Doppler evaluation of the longitudinal free wall or septum on apical four-chamber views of the heart. The advantage to deriving the MPI using TDI is that the same cardiac cycle can be used since TDI records myocardial motion during systole and diastole wherever the pulsed-wave gate is placed. Tissue Doppler MPI may help overcome errors in evaluation secondary to variations in heart rate when PW is used at different points in time.

Intervals used for the calculation of the MPI using Tissue Doppler: IVRT= isovolumic relaxation time, IVCT = isovolumic contraction time, ET = left ventricular ejection time, S′ = systolic myocardial motion, E′ = early diastolic myocardial motion, A′ = late diastolic myocardial motion.

59
Q

What are additional advantages to utilizing PW-left ventricular MPI?

A

Most studies have shown pulsed-wave derived left ventricular MPI to be independent of heart rate, blood pressure, body weight, body surface area, sex, and age in dogs and cats. Right ventricular Tei index is also unaffected by age, heart rate, and body weight.

60
Q

True or False. Tei index appears to be preload and BP dependent and is not affected by acute changes in loading conditions

A

False. The Tei index appears to be preload and BP independent, BUT IS significantly affected by acute changes in loading conditions.

In dogs with mitral regurgitation secondary to degenerative valve disease, the Tei index remained normal unless systolic dysfunction was present. It is a sensitive indicator of acute increases in afterload, however, which causes the Tei index to INCREASE.

61
Q

What does increased values for MPI indicate?

A

Increased values for both right and left ventricular MPI are indicative of myocardial dysfunction when changes in load are chronic.

62
Q

Like the 4-types of values that Tissue Doppler can acquire when measuring for systolic myocardial function.

A

Tissue Doppler time intervals associated with systolic myocardial function include:

  1. Q–S’ (the time interval from the beginning of the QRS complex to the beginning of S’)
  2. Q–peak S’ (the time interval from the beginning of the QRS complex to peak velocity of S’)
  3. Q–end S’ (the time interval from the beginning of the QRS complex to the end of S’)
  4. Duration of S’

There are significant INVERSE relationships between Q–S’ and ejection fraction and between Q–end S’ and ejection fraction, and a significant POSITIVE relationship between ejection fraction and duration of S’.

NOTE: These TDI indices are heart rate affected, and all of these time intervals should be corrected for heart rate (dividing the parameter by the square root of the R-to-R interval).

63
Q

What components contribute to diastolic function of the heart?

A
  1. Myocardial relaxation
  2. Atrial contraction
  3. Rapid and slow filling phases
  4. Loading conditions
  5. Pericardial sac.
  6. Elastic properties of the heart.
64
Q

When does left ventricular chamber filling occur?

A
  1. Rapid ventricular filling phase (E-wave?)
  2. A slow ventricular filling phase (Diastasis)
  3. Filling secondary to atrial contraction (A-wave)
65
Q

List some diastolic filling abnormalities that may occur secondary to impaired or delayed relaxation or decreased compliance within the left ventricle.

A
  1. When relaxation is impaired, left ventricular pressure remains high early in diastole, and left ventricular filling is delayed until later in the diastolic time period resulting in a greater contribution to left ventricular filling from the atrial contraction.
  2. Compliance of the heart is a reflection of its distensibility. A compliant ventricular chamber allows proper filling at normal pressure while a noncompliant ventricular chamber is stiff, and pressure elevates rapidly as the chamber fills.
  3. Compliance plays a larger role in late diastole when the ventricular chamber is already partially filled. Hypertrophy and ischaemia are primary factors affecting relaxation, while fibrosis, infiltrative processes, hypertrophy, and other structural abnormalities are the primary factors affecting compliance of the heart.
66
Q

What might be the consequences of impaired diastolic function?

A

Impairment of diastolic function can produce backward or forward heart failure. Forward failure results from decreased ventricular volume secondary to restricted filling. Backward failure is the result of high left ventricular filling pressure reflected back into the left atrium.

67
Q

What are other factors that directly affect ventricular filling?

A

Other factors affecting ventricular filling include heart rate and rhythm and left atrial function. Rapid heart rates limit adequate left ventricular filling since early rapid filling and late diastolic filling phases coincide. Poor atrial function also diminishes late diastolic filling.

68
Q

List parameters to assess diastolic function.

A
  1. Isovolumetric relaxation time
  2. Pulmonary vein flow
  3. transmitral valve flow
  4. TDI - E’ and A’
69
Q

How does LA size affect left ventricular diastolic function?

A

LA size is influenced by left ventricular diastolic function and can be considered a morphologic expression of diastolic function, rather than a direct measurement. It is also important as it has prognostic implications; increased LA size is associated with increased risk of congestive heart failure (CHF), as well as thromboembolic disease. LA size can be assessed by diameter or volume. In clinical practice, diametric measurements are used more commonly, as they are faster and more repeatable.

70
Q

How does transmitral flow affect left ventricular diastolic function?

A

Probably the most important measurement for assessing diastolic function and filling pressures. It is measured from the left apical four chamber view, using pulsed wave Doppler to evaluate blood flowing into the left ventricle. There are two phases of left ventricular filling, the early (E) wave, which corresponds to the rapid filling phase of diastole and the atrial (A) wave, which corresponds to the atrial contraction (booster) phase. There are four important patterns of transmitral filling.

71
Q

Describe the NORMAL relaxation pattern, in the assessment of diastolic function.

A

A normal relaxation pattern is one in which the E wave is taller than the A wave, with the E:A ratio being between 1-2, reflecting the fact that under normal circumstances early filling comprises the majority of LV filling.

72
Q

Describe the IMPAIRED relaxation pattern, in the assessment of diastolic function.

A

With early diastolic dysfunction there is less passive filling and the E wave becomes smaller than the A wave; this is termed impaired relaxation. This can be normal in elderly patients.
It is characterized by:

  1. Reverse E:A ratio (<1)
  2. Slow MV deceleration
  3. Long IVRT
73
Q

Describe the PSEUDONORMAL relaxation pattern, in the assessment of diastolic function.

A

As diastolic function worsens the left atrial pressure increases and the E wave once more becomes taller than the A wave. This is called pseudonormal filling, as the E:A ratio is normal/looks normal, however significant diastolic dysfunction is present.

Normal and pseudonormal filling cannot be distinguished on transmitral flow alone and TDI and pulmonary venous flow are often needed to define the pattern.

74
Q

Describe the RESTRICTIVE relaxation pattern, in the assessment of diastolic function.

A

Finally in severe diastolic dysfunction the markedly elevated LA pressures result in fast, short early filling. The A wave is small, reflecting the fact that most filling is achieved by the E wave. LA function is often reduced as well, which contributes to the small A wave. This is called restrictive filling. The E:A ratio in restrictive filling is greater than 2.

75
Q

How does IVRT affect left ventricular diastolic function?

A

This is the time in the cardiac cycle between aortic valve closure and mitral valve opening and lasts around 40-60ms in normal cats.

With impaired relaxation the IVRT increases – this can be seen in preclinical disease. The other factor that affects IVRT is LA pressure; as LA pressure increases, IVRT shortens.

In more severe conditions the increased LA pressure predominates and IVRT shortens. IVRT is also reduced by tachycardia, though not usually to the same extent as by disease.

76
Q

How does E-Wave Deceleration affect left ventricular diastolic function?

A

This is mainly determined by left ventricular stiffness. It is prolonged in impaired relaxation, and shortens as diastolic function worsens and progresses towards being more restrictive. This isn’t a very repeatable measurement, however, and the reference range is wide, between 45-100ms, likely due to high heart rates. As such, it is a less helpful variable and is never used on its own.

77
Q

How does Pulmonary venous flow affect left ventricular diastolic function?

A

PVF is triphasic, comprising of a systolic (S) wave, a diastolic (D) wave and an atrial reversal (Ar) wave.
- The S wave is determined by both left ventricular systolic function and left atrial relaxation. In patients with significant mitral regurgitation the turbulent flow will often obscure the pulmonary venous flow in systole.
- The D wave is similar to the transmitral E wave in its physiology; it is determined by left ventricular relaxation and left atrial pressure.
- The Ar wave is a negative wave, below the baseline, reflecting LA booster pump function, as well as left atrial afterload.

PVF is normally systolic-dominant, with a taller S wave then D wave.

In pseudonormal and restrictive filling the S wave becomes smaller and the D wave becomes bigger. This is one way by which normal and pseudonormal filling can be differentiated. In pseudonormal and restrictive filling the duration of the transmitral A wave becomes shorter than the duration of the Ar wave (Ar/A>1). Furthermore, the Ar wave velocity reduces as left atrial function reduces.

78
Q

The transmitral E wave velocity is indexed to another variable, usually IVRT or the Tissue Doppler E’. What’s the theory for indexing to E’?

A

The E wave is influenced by both filling pressure and relaxation, by indexing it to E’, which is largely relaxation-dependent, it corrects for the effect of relaxation.

As filling pressures increase, E increases, E’ reduces, and therefore, E:E’ increases \

<12 is normal in cats.

79
Q

Why is E:IVRT more preferred in dogs then cats?

A

In dogs, E:IVRT has been found to be more accurate for the prediction of increased filling pressures and congestive heart failure; it’s not validated in cats.

E:IVRT >1.8 DCM
E: IVRT >2.5 MMVD