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4. Physiology and pathophysiology > Systolic function > Flashcards

Systolic function Flashcards

1
Q

What are systolic time intervals

A
  • Accurate to assess LV performance
    o Better indicators of LV systolic function (vs FS%)
    o Not indicator of contractility
  • Measure the sequential phases of ventricular systole
    o LV ejection time (LVET): from start to end of ejection
    o LV pre-ejection period (PEP): onset of QRS/depol => start of ejection
    o Velocity of circumferential shortening (Vcf)
     Reflect rate of LV shortening
    o LV ejection to pre-ejection period ratio (LVET/PEP)
     Calculated to decr HR influence
     Combine in 1 parameter  indicator of myocardial performance
    o Total electromechanical systole: onset of QRS => AoV closure (2nd heart sound) = PEP + LVET
     Insensitive to decr contractility, preload changes
     Influenced by afterload
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2
Q

STIs will be affected by

A

by HR and loading conditions
o STI can be corrected for HR: STI x HR x (slope of regression of HR vs STI curve)
 Short cycle length (incr HR): underestimate LV perform.

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3
Q

Formula for Vcf

A

LVIDd-LVIDs/LVIDd x LVET

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4
Q

Influence of contractility on STIs

A
  • incr PEP => decr rate of pressure rise (dP/dt)
  • incr PEP/LVET
  • decr LVET
  • Normal or decr Vcf
  • Normal QAVC
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5
Q

STIs: incr preload

A
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6
Q

incr preload and decr afterload mimic

A

incr contractility => decr PEP, incr LVET => decr PEP/LVET

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7
Q

decr preload and incr afterload mimic

A

decr contractility => incr PEP, decr LVET => incr PEP/LVET

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8
Q

Effects of afterload and contractility on LVET

A

Incr of decr afterload => incr LVET

Incr or decr contractility => decr LVET

Less useful for eval of myocardial failure or effect of inotropic tx

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9
Q

STIs: incr afterload

A

incr PEP from incr heart work => longer time to reach pressure in LV before AoV open

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10
Q

STI decr afterload

A

: LV function is easier
 decr PEP: force to reach pressure is shorter
 incr VCF: rate at which the heart contract is faster

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11
Q

STI incr preload

A

 volume in the heart => Starling mechanism => incr contractility
 decr PEP, incr LVET

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12
Q

STI decr preload

A

not allow force to be generated = incr PEP

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13
Q

STIs effect of HR

A

inversely related to LVET, no/little effect on PEP
o incr HR => decr LVET + incr PEP
o decr HR => incr LVET + decr Vcf

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14
Q

STI MR

A

incr PEP
decr LVET
incr PEP/LVET

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15
Q

STI SAS

A

decr PEP
incr LVET
decr PEP/LVET

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16
Q

Catecholamines

A

incr contractility and HR
decr PEP
decr LVET
decr PEP/LVET
decr QAVC
incr Vcf

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17
Q

What prolongs PEP

A

decr preload
incr afterload
decr myocardial fct
neg inotropes

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18
Q

What shortens PEP

A

incr preload
decr afterload
positive inotropes

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19
Q

What prolong LVET

A

incr preload
incr afterload
decr afterload
decr HR

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20
Q

What shortens LVET

A

decr preload
positive inotrope
negative inotropes
incr HR

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21
Q

What incr PEP/LVET

A

decr preload
neg inotropes
decr myocardial fct
incr HR

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22
Q

What decr PEP/LVET

A

incr preload
decr afterload
decr HR
Positive inotropes

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23
Q

What prolong QAVC

A

decr HR
incr afterload
neg inotropes

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24
Q

What shortens QAVC

A

incr HR
pos inotropes

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25
Q

What incr Vcf

A

decr afterload
decr myocardial fct
incr HR
pos inotropes

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26
Q

What decr Vcf

A

incr afterload
decr HR
neg inotropes

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27
Q

STIs CM

A

incr PEP
decr LVET
incr PEP/LVET
normal QAVC
decr Vcf

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28
Q

STIs VSD

A

incr PEP
decr LVET
incr PEP/LVET
— QAVC
— Vcf

29
Q

STIs R CHF

A

incr PEP
decr LVET
incr PEP/LVET
— QAVC
— Vcf

30
Q

STI hypoT4

A

incr PEP
decr LVET
incr PEP/LVET
— QAVC
— Vcf

31
Q

STIs hyperT4

A

decr PEP
incr LVET
decr PEP/LVET
— QAVC
— Vcf

32
Q

STIs diabetes

A

incr PEP
decr LVET
incr PEP/LVET
— QAVC
— Vcf

33
Q

STI digitalis

A

decr PEP
—- LVET
decr PEP/LVET
— QAVC
incr Vcf

34
Q

STI propanolol

A

incr PEP
NA LVET
incr PEP/LVET
— QAVC
— Vcf

35
Q

STI hydralazine

A

decr PEP
incr LVET
decr PEP/LVET
— QAVC
— Vcf

36
Q

What is LV dp/dt

A
  • Clinical index of contractility
  • Rate of LV pressure rise: dp/dt
    o Load independent measure of LV contractility
    o Occur during IVCT = isovolumic period → after/preload constant
37
Q

What affects LV dp/dt

A

o Intrinsic myocardial contractility
o Mechanical dyssynchrony may  dp/dt
 ie BBB
o ↑ preload can affect contractility fron Starling’s law

38
Q

Measure of LV dp/dt

A
  • Non invasively with MR jet
    o LA pressure do not change significantly during IVCT
     AoV + MV closed
     Load independant
    o Time from 1m/s => 3m/s divided by 32mmHg
     Represent pressure change of 32mmHg according to Bernoulli equation
    o Average dp/dt over that period
    o Generally underestimated
  • Invasively by heart catheterazation
    o Micromanometer tip KT in chamber
39
Q

What affects ejection phase indices

A

by contractility, pre and afterload
o incr preload => incr ejection phase indices (MR, AI, anemia…)
o decr afterload => decr ejection phase indices

40
Q

What is assessed by ejection phase indices

A
  • Not indicative of LV contractility
  • Clinical measurement of LV systolic fct
41
Q

Parameters of ejection phase indices

A

FS%
Thickening fraction
Vcf
EPSS
VTI of Ao flow

42
Q

3D volumetric equivalents of ejection phase indices

A
  • Ejection fraction (EF%): % of end diastolic volume ejected w each beat
    o Normal <0.4, severe depression of LV function <0.2

EF (%) = (EDV - ESV)/EDV x 100

  • Mean normalized ejection rate: indexes the EF to LVET

E rate = (EDV - ESV)/(EDV x ET)

  • Cardiac output (CO):
    o Insensitive indicator of cardiac performance => many compensatory mechanisms will aim to maintain CO in cardiac dz

o SV: estimated by calculating LV volumes (diastolic – systolic) or blood flow velocity in great vessels
CO = SV x HR

43
Q

What is LV FS%

A
  • Change in dimension from end diastole => end systole
  • Normal values => dogs: 25-45%, cats: 30-55%

FS (%) = (LVIDd - LVIDs)/LVIDd x 100

44
Q

What is thickening fraction

A
  • % of change in LVFW or IVS thickness
  • Useful when heterogenous myocardial performance
45
Q

What is Vcf

A

Velocity of myocardial fiber shortening (Vcf)
* Rate of change in LV circumference
o End diastolic endocardial circumferential length  end systolic
* Normal values: dogs: 1.6-1.8 circ/s

Vcf = (LVIDd - LVIDs)/(LVIDd x ET)

46
Q

What is EPSS

A

Mitral E point to septal separation (EPSS)
* Max initial opening of MV => normal values = dogs: <6mm, cats: <4-5mm
o Inversely proportional to LA => LV flow
o Indicator of LV dysfunction

47
Q

What is VTI Ao flow

A
  • Area under the systolic ejection curve
  • Correlates to SV if AoV diameter is constant
48
Q

Major determinants of systolic function

A

Preload
Afterload
Contractility
HR

49
Q

How does preload affect systolic fct

A
  • Load before the contraction has started = force stretching the myocardium
  • Provided by venous return
    o incr preload => ventricular distension => incrSV
    o Starling’s law: incr stretch of myocardial fibers => incr ventricular performance
     incr contraction velocity and force
     Optimal overlap of actin and myosin
     Enhanced sensitization of actin-myosin to Ca2+ transient
  • Hypertrophy pattern: eccentric
50
Q

How does afterload affect systolic fct

A
  • Load after the ventricle starts to contract
  • Determined by
    o Arterial blood pressure
    o Aortic compliance: Ao pressure/Ao flow
     Varies throughout systole
  • incr afterload
    o incr intraventricular pressure => incr wall stress
    o stimulates sarcolemma stretch => incr intra¢ [Ca2+]
  • Wall stress: tension (force that tend to pull apart) applied to a CSA
    o Law of Laplace: see figure
    o incr wall thickness will compensate incr pressure/volume
    o incr radius (chamber dilation) => incr wall stress
  • Peak force developed pressure: total # of cross bridges since start of systole=> depend on
    o Initial fiber length
    o Systolic Ca2+ incr
    o Ca2+ responsiveness of myofilaments
    o Myosin light chain phosphorylation
    o Loading
  • Hypertrophy pattern: concentric
51
Q

How does contractility affect systolic fct

A
  • Inotropic state
  • Important regulator of O2 uptake
  • incr interaction of Ca2+ and contractile proteins
    o incr Ca2+ transients
    o Sensitization of contractile proteins to Ca2+
  • Maximal velocity of contraction (Vmax or V0)
    o incr with symp activation
    o Proportional to:
     Myosin ATPase activity
     Rate limiting steps in cross bridge cycle
     Rate of incr and peak level of cytosolic Ca2+
  • Maximal tension (P0): related to # of attached cross bridges and peak Ca2+
52
Q

How does HR affect systolic fct

A
  • Acute regulation of contractile state (w Frank Starling and autonomic control)
  • Determinant of myocardial O2 demand (w myocardial wall stress and contraction velocity)
    o Force frequency relationship (= positive inotropic effect of activation)
     Bowditch staircase or Treppe effect
     incr HR => incr contractility and force of ventricular contraction
     incr Na+ and Ca2+ influx => overwhelme Na+/K+ pump => incr [Na+] => activation of Na+/Ca2+ exchanger => Ca2+ influx => incr [Ca2+]
53
Q

Particularities of RV systolic fct

A
  • 3 systolic phases:
    o Contraction of papillary muscles
    o Mvt of RVFW => IVS
    o Wringing of the RV 2nd to LV contraction
  • Contraction starts at the apex => thin walled/compliant upper region
    o Slow and continuous blood flow into lungs
  • Shorter IVRT/IVCT
  • Longer ET
54
Q

Clinical indices of myocardial contractility

A

Isovolumic indices: dP/dt

Load sensitive indices:
- EF% FS%
-Vcf

End systolic indices
End systolic volume
end syst PV relationship
end syst wall stress

PV loops

TDI: IVCT

55
Q

Clinical indices of myocardial contractility

A

LV fct curves
Maximal rate of LV pressure generation
Ejection phase indices
Volumetric flow
Myocardial performance index
Tissue Doppler indices

56
Q

Invasive assessment of systolic fct

A
  • KT based methods: end systolic elastance (Es), +dT/dP
  • Indicator dilution methods: thermodilution, indocyanine green, Fick, lithium dilution
  • Imaging: SPECT, cineangiography, radionuclide angiography, MRI, SPECT
57
Q

Non invasive assessment of systolic fct

A
  • M-mode/2D
    o LVIDd, EPSS
    o LV volume: SMOD
    o Load dependent indices: FS, EF, Vcf, SV, CO
    o Wall stress
  • Doppler
    o E wave: decr if decr CO
    o dP/dT of MR
    o Tei index: (IVCT-IVRT)/ET
    o LV dP/dT
    o STIs : PEP, LVET, PEP/ET
  • TDI
    o Pulse wave S wave
    o Strain, strain rate
    o Speckle tracking
  • RV function
    o Tricuspid annular motion
    o Myocardial performance indices
    o CaVC imaging
    o TR => PAPs
58
Q

Left ventricular function curves

A
  • Obtain with IV infusion => vary end diastolic volume => repetitive measures
    o Swan-Ganz KT: pulmonary wedge pressure as surrogate of heart volume/end diastolic fiber length
  • Based on Starling relationship
  • Pressure volume loops:
    o As preload incr => volume incr => incr contractility =>icnr SV => decr end systolic volume at similar end systolic pressure
    o incr slope of end systolic pressure volume relationship
59
Q

Maximal rate of LV pressure generation

A
  • During IVCT: constant preload/afterload
    o Maximal rate of pressure generation = index of inotropic state
    o Inotropic index = max dP/dt
  • Preload can still influence by incr contractile state with incr length activation
  • LV KT necessary (transducer tipped KT)
    o If MR present => can assess LA/LV pressure gradient
60
Q

Ejection phase indices

A

EF
FS
Vcf
Ejection phase indices
MV and TV annular motion

61
Q

Calculation of EF

A

relates stroke volume to end diastolic volume
o Index of the extent of LV fiber shortening
o Relates systolic emptying of the end diastolic volume, but no information about this volume
 Does not imply forward SV
 Measure of volume leaving LV (MR, shunt…)
o Determined by volume measurements
 Teicholz method: assume LV as an ellipse
* LV overload => changes LV geometry to more spherical shape
* Normal according to BSA:
o Systolic <30ml/m2
o Diastolic <100ml/m2
 Simpson’s rule: best correlation w actual LV volumes
* Unaffected by changes in geometry
* Computerized calculation of volume from stack of discs from LAX planes in systole and diastole
* Volume = 0.85 A2/L
* Normal according to BSA: systolic <30ml/m2 , diastolic <70ml/m2
 Bullet methods: assume bullet shaped ventricle
* Transverse images at level of chordae + length on LAX
* LVV = 5/6 x area x length

62
Q

Calculation of FS

A

% of change of LV chamber size in systole
o Measure of contractility, not function
o Factors affecting: contractility, afterload, preload
 decrFS% => decr contractility, decr preload, incr afterload

63
Q

Calculate Vcf

A

velocity of circumference change in systole
o Minor axis: distance from the L side of IVS => LVFW
o incr afterload => decr Vcf: slower contraction rate

64
Q

MV and TV annular motion

A

o Correlated to EF%: decr if decr EF
o Normal in dogs:0.46 to 1.74cm
 Influenced by BW => can be indexed on BSA
o TAPSE: TV
 Poorer px in Hu w L-CHF 2nd to DCM or PH

65
Q

Volumetric flow

A
  • Continuity equation: volume in = volume out
    o Flow profile: area under the curve = VTI
    o Area of the vessel

VTI = (Velocity x ET)/2
CSA = πr2
SV = VTI x CSA

66
Q

Myocardial performance index

A
  • Global myocardial function => correlates w diastolic + systolic fct
  • Preload and BP independent
  • Affected by acute changes in loading conditions

MPI = (IVRT - IVCT)/ET

67
Q

Tissue Doppler

A
  • Systolic wave (S’) and diastolic waves (E’ and A’)
  • Q-S’: time from start of QRS => S’
68
Q

Contrast contractility vs. systolic function, what is the difference?

A
  • Contractility is an inherent property of the myocardium
  • Systolic function is the performance of the myocardium, and can be affected by several factors

4. Physiology and pathophysiology (18 decks)

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