The heart pump Nov1 M2 COPY Flashcards

1
Q

what S1 (1st heart sound) corresponds to

A

closure of the AV valves (tricuspid and mitral) during systole

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2
Q

what S2 corresponds to

A

closure of seminular valves (aortic and pulmonic) at start of diastole and start of isovolumetric relaxation

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3
Q

seminular valves (2)

A

aortic and pulmonary valve

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4
Q

S3 corresponds to what

A

heart sound when ventricular filling at diastole when blood hits the ventricle wal

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5
Q

S3 heard where (2)

A

individuals with very good diastole or indiv. with heart failure

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6
Q

why hear S3

A

because vacuum created by ventricle relaxation

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7
Q

ventricle relaxation passive or active

A

active (ATP dependent). put calcium back in SR

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8
Q

S4 corresponds to what

A

atrial contraction when pumps blood in stiff ventricle (non compliant)

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9
Q

S4 heard where

A

abnormal (pathologic) in patients with non compliant ventricle

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10
Q

if had 4 heart sounds, in what order would hear them

A

S1, S2, S3, S4

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11
Q

pressure volume loop. how to get that

A

plot left ventricular pressure as a function of ventricular volume

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12
Q

pressure volume loop 1st part (out of 4)

A

mitral valve opens, ventricle fills slowly (go to right, increase in volume and slight increase in P) until EDV

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13
Q

pressure volume loop 2nd part

A

isovolumetric contraction. pressure rises but volume stays the same (vertical rise)

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14
Q

pressure volume loop 3rd part

A

aortic valve opens, ejection, ventricular volume falls to ESV. pressure rises but falls back a little

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15
Q

pressure volume loop 4th part

A

from ESV, isovolumetric relaxation. vertical drop in P without change in volume. until mitral valves open

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16
Q

why ventr pressure goes up when filling (increasing volume)

A

bc even though ventricles stretch, limited by pericardial cavity

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17
Q

ESPVR def

A

end systolic pressure-volume relationship. (P and V relationship in ventricle at end of systole)

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18
Q

ESPVR is an indicator of what

A

how strong the heart is

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19
Q

ESPVR: what determines the moment when systole ends

A

is when aortic valve closes (when P aorta = P ventricle)

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20
Q

EDPVR stands for what and what it does

A

end diastolic pressure-volume relationship. (P ventr as function of ventr. volume during filling of ventricle)

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21
Q

EDPVR shape

A

follows first part of pressure volume loop and extends a bit higher and further to the right

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22
Q

length-tension relationship or cardiac muscle length-tension cycle: what it is

A

ventricular muscle tension as a function of muscle length

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23
Q

what curve does cardiac muscle length-tension cycle ressemble and why

A

the pressure volume loop bc ventricular volume and muscle length are related linearly

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24
Q

how to see stroke volume on a PV loop

A

right vertical line minus left vertical line (EDV - ESV)

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25
Q

3 determinants of stroke volume

A

preload, afterload and contractility

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26
Q

preload def and effect

A

EDV. Greater EDV gives greater muscle contraction (Frank-Starling’s law)

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27
Q

how increased preload affects PV loop

A

1st portion ends at greater vol and higher P. Shifts the right part of the graph to the right. But all comes back to same ESV so greater stroke volume

28
Q

how to increase preload (practically speaking)

A

squeeze capacitance veins, IV injection of fluid, receive blood

29
Q

afterload two definitions

A
  • pressure against which the heart contracts

- left ventricular wall stress during ejection

30
Q

wall stress formula

A

ventr P x radius of ventr. div. (2 x wall thickness)

31
Q

afterload is proportional to __________

A

left ventricular pressure

32
Q

left ventricular load is considered to be _______

A

systolic arterial BP (diast BP + third of pulse pressure)

33
Q

why consider that afterload is the MAP

A

bc normally, left ventricle systolic P = systolic arterial BP and aortic valve open

34
Q

how increased afterload affects the PV loop

A

the 2nd portion (vertical isovol contraction) goes higher bc fighting against greater P so afterload is greater. P raises and falls back at ESPVR at greater volume so ESV increased

35
Q

why greater aortic pressure leads to greater afterload

A

have to push harder to open the aortic valve

36
Q

consequence of greater afterload on SV

A

SV reduced bc EDV unchanged and ESV increased

37
Q

why ESV increases when afterload increased

A

greater afterload results in less shortening of the ventricle

38
Q

2 clinical conditions where find high afterload

A

hypertension, aortic valve stenosis

39
Q

contractility def

A

inherent strength of heart’s contraction

40
Q

SS effect on tension-length cycle

A

shifts the curve upwards (for same muscle length, greater tension)

41
Q

SS on PV loop

A

shifts ESPVR curve up and to the left (and is curved to the left a little). ESV is now lower (left part of the curve is now more to the left)

42
Q

SS effect on SV and why

A

increased bc ESV decreased

43
Q

ejection fraction formula + normal values

A

Stroke volume div. EDV x 100.

Normal EF: 55-70%

44
Q

CO formula and determinants

A

CO=HR x SV

45
Q

how body changes HR

A

SS and PSS affect the diastolic depolarization of the SA node

46
Q

name of effects affecting HR and what we call it when SS vs PSS

A

chronotropic effects.
SS: positive chronotropic effect
PSS: negative chronotropic effect

47
Q

name of effects affecting SV and 3 things that can do that

A

inotropic effects. (preload, afterload, contractility)

48
Q

what we call the effect when preload, afterload and contractility increases

A

increased preload: positive inotropic effect
increased afterload: negative inotropic effect
increased contractility: positive inotropic effect

49
Q

cardiac function curve plots what

A

CO as a function of cardiac filling pressure

50
Q

how SS and PSS affect the cardiac function curve

A

shift it up or down

51
Q

example of thing increasing cardiac filling (moving up on the cardiac function curve)

A

increased preload

52
Q

cardiac output or cardiac function curve in the right atrium: plots what + shape

A

CO as function of right atrial P. sigmoidal shape. reach plateau at 3 mmHg and 12.5 L per min.

53
Q

what shifts the right atrium cardiac function curve upwards

A

increased HR, contractility and decreased afterload (decreased BP and TPR)

54
Q

right atrium cardiac fct curve shifted down is said to be ______ and shifter up is called _______

A

hypoeffective vs hypereffective

55
Q

give 3 main imaging techniques to assess cardiac function and CO

A

Echography (ultrasound), cardiac angiography, radionuclide ventriculography (or MUGA: multigated acquisition scan)

56
Q

how cardiac angiography works

A

catheters placed in right or left ventricle, inject radio-opaque medium

57
Q

how radionuclide ventriculography works

A

IV injection of radioactive isotope, binds to RBCs, measure intensity of radiation at ventricles during cardiac cycle

58
Q

other heart imaging technique to assess cardiac function and CO

A

PET scans, CT angiograms, cardiac MRI

59
Q

Fick’s principle (gross formula)

A

amount of substance consumed by an organ is equal to blood flow rate x (what goes in organ - what goes out organ)

60
Q

application of Fick’s principle to get CO

A

CO = oxygen consumed by the lung div (arteriol O2 - mixed venous O2). (200 div by (200-160))

61
Q

To apply Fick’s principle, how to get O2 consumed

A

special machine for that

62
Q

To apply Fick’s principle, how to get arterial O2

A

puncture in any artery

63
Q

To apply Fick’s principle, how to get mixed venous O2

A

catheter to go to pulmonary artery or right ventricle

64
Q

normal values in the calculation of CO using Fick’s principle

A

200 div. (200 - 160) = 5L per min

65
Q

thermodilution method used for what

A

measuring CO

66
Q

thermodilution method principle

A

saline of known temperature injected through catheter in right atrium. tip of catheter in pulm artery registers Temp change. CO can be calculated

67
Q

how thermodilution results presented and interpreted

A

graph of amount of cold as function of time. greater surface area: lower CO. smaller SA: greater CO