Lec 14-15 Cardiac Cycle Flashcards

1
Q

How do preload and afterload affect cardiac output?

A
  • high preload = increased cardiac output

- higher afterload = decreased cardiac output

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2
Q

How does Ca affect contraction strength?

A

small ca induced ca release [CICR] –> weak contraction

large CICR –> strong contraction

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3
Q

What two things does contraction strength depend on?

A
  1. Ca release

2. initial length [preload]

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4
Q

2 factors in force-length relation in intact heart?

A
  1. ventricular filling from veins/atria pre-stretches the ventricles [preload]
  2. ventricles must contract against existing arterial pressure [afterload]
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5
Q

When are LVP and aortic pressure closest?

A

at their peak, just at end of QRS is ST interval

LVP still > than aortic pressure

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6
Q

What causes mitral valve to open? to close?

A

open: LAP > LVP
close: LVP > LAP

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7
Q

What changes to pressure and volume between mitral valve closure and aortic valve opening?

A
  • LVP gets bigger, volume stays the same = isovolumic contraction
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8
Q

What causes aortic valve to open? to close?

A

opens: when LVP > aortic pressure
closes: aortic P > LVP

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9
Q

What is happening to pressure and volume in left ventricle during ejection?

A
  • pressure and volume both changing
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10
Q

What kind of relaxation in LV after aortic valve closes?

A

isovolumic relaxation

- volume is flat, pressure changes

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11
Q

What is first heart sound? and second?

A

first: closing AV valves [QRS wave]
second: closing aortic and pulmonary valves [just after T wave]

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12
Q

3 important principles illustrated by wiggers diagram?

A
  1. atrial P is low, Ventricular/aortic P is high
  2. valves only open when upstream P > downstream P
  3. heart sounds correspond to discrete events
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13
Q

Where are the 4 valves located [and names]

A

AV valves
tricuspid: RA –> RV
mitral [bicuspid]: LA –> LV

semi-lunar valves

pulmonary: RV –> pulm artery
aortic: LV –> aorta

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14
Q

Why are valves so important?

A

ensure unidirectional blood flow

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15
Q

4 phases of PV loop [including valve events]

A
MV closes
1. isovolumic contraction
Aortic V opens
2. ejection
Aortic V closes
3. isovolumic relaxation
MV opens
4. diastolic filling
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16
Q

How to get SV [stroke volume] from EDV and ESV?

A

SV = EDV - ESV

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17
Q

How to get EF [ejection fraction] from SV and EDV?

A

EF [ejection fraction] = SV/EDV

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18
Q

What is the EDPVR? linear or non-linear?

A
  • end-diastolic pressure-volume relationship
  • nonlinear
  • defines the lower boundary for end-diastolic P-V point of PV loop
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19
Q

What does the slow of the EDPVR mean?

A

on P-V graph: x axis = V, y axis = P
flatter = more compliant
steeper = less compliant

20
Q

What does EDPVR nonlinearity mean?

A

low volume: small slope, ventricle compliant, easy to fill

high volume: large slope, ventricle stiff, difficult to fill

21
Q

What is the ESPVR? linear or non-linear?

A
  • end-systolic pressure-volume relationship

- linear

22
Q

What do EDPVR and ESPVR do together?

A

define boundaries within which PV loop sites

independent of preload and afterload

23
Q

Do EDPVR/ESPVR depend on preload and afterload?

A

No, they are independent

24
Q

What is the preload? Two common ways to measure it? What point is it on PV loop?

A
  • the load imposed on ventricle at end of diastole
  • measured as end-diastolic volume [EDV] or end-diastolic pressure [EDP]
  • the bottom right corner on PV loop
25
Q

With constant afterload and contractility, how does preload affect SV and arterial BP?

A

increased preload –> increased SV and arterial BP

26
Q

What is frank starling curve [x and y axes]? what relation does it show?

A

x axis: LVEDP or LVEDV or right atrial pressure or venous pressure
y axis: stroke volume or CO
it shows that increased preload –> increased output

27
Q

What 2 things increase preload?

A
  • fluid retentions [in advanced heart failure]

- constriction of veins

28
Q

What 2 things decrease preload?

A
  • blood loss

- dilation of veins

29
Q

What is afterload? Common way to measure it?

A
  • mechanical load of ventricle during ejection
  • normally determined by arterioles
  • Commonly measured at TPR
30
Q

What is equation for TPR?

A

TPR = MAP/CO

31
Q

What are 2 effected of increased TPR when constant preload and contractility?

A
  • increased pressure

- decreased SV

32
Q

What 3 things can increase afterload?

A
  • temporary constriction of arterioles
  • chronic hypertension
  • aortic stenosis [valve narrowing or blockage]
33
Q

What 1 thing decreases afterload?

A

dilation of arterioles

34
Q

What will negative inotropic agent do to ESPVR?

A

ESVPR will have less steep slope

35
Q

What will positive inotropic agent do to ESPVR?

A

ESVPR will have steeper slope

36
Q

What is Ees? what changes it?

A
  • slope of ESPVR
  • its the index of ventricular contractility
  • inotropic drugs change it –> pos inotropic drugs increase it, negative inotropic drugs decrease it
37
Q

What 3 things increase contractility?

A
  • B adrenergic stimulation in ventricle
  • increased plasma Ca
  • increase in muscle mass [physiological hypertrophy]
38
Q

What 4 things decrease contractility?

A
  • B adrenergic receptor blockers
  • Ca channel blockers
  • decreased energy supply [ischemia or hypoxia]
  • decreased muscle mass [MI]
39
Q

Does increased SV indicate an increase in contractility?

A
  • NOPE – Not by itself
40
Q

What 3 things things can increase SV?

A
  • increased contractility
  • increased preload
  • decreased afterload
41
Q

What is clinical contractility index?

A

ejection fraction [EF]

42
Q

What is equation for ejection fraction?

A
EF = SV/EDV
SV = stroke volume, EDV = end diastolic v
43
Q

Does afterload affect EF?

A

Yes, significantly

44
Q

Does preload affect EF?

A

yes minorly

45
Q

does contractility affect EF?

A

yes!