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Cardiology > Cardiac Control 1, 2, and 3 -Cardiac Output and Arterial Pressure > Flashcards

Cardiac Control 1, 2, and 3 -Cardiac Output and Arterial Pressure Flashcards

1
Q

Degree of myocardial stretch during diastole is determined by what interaction?

A

diastolic pressure and chamber compliance (measured by chamber architecture and myocardial properties)

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2
Q

At upper ranges, a given increment in LVEDP produces a larger/same/smaller increment of LV end diastolic volume.

A

smaller –> myocardial diastolic force-length relationship is non linear

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3
Q

During ventricular contraction, which myocytes shorten the most and contribute the most to cavity volume reduction?

A

subendocardial myocytes shorten more than the epicardial surface

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4
Q

The load that ventricular muscle must overcome during systole to eject.

A

Ventricular afterload

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5
Q

How is the extent of cardiac muscle shortening during systole related to the load opposing it?

A

inversely –> increasing afterload decreases extent to which cardiac muscle can shorten, thereby decreasing stroke volume

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6
Q

T/F as a ventricle ejects during systole, the wall force increases as pressure increases and the ventricle volume decreases

A

F –> b/c volume goes down, wall force goes down despite pressure increase (a larger ventricle has larger wall force) –> AKA the ventricle has to produce less force to maintain the same/greater pressure outflow

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7
Q

At what point is systolic wall stress greatest?

A

at onset of ejection as ventricular volume is largest

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8
Q

During ejection LV pressure increases in the first half of systole and wall stress increases/decreases –> why?

A

decreases b/c of larger effect of decrease in LV dimension

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9
Q

What is the increased inotropic state of cardiac muscle?

A

cardiac muscle can increase force at any given length

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10
Q

What determines ventricular stroke volume?

A

EDV-ESV

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11
Q

What determines EDV?

A

preload as measured by EDP and diastolic force-length relationship

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12
Q

What determines ESV?

A

Afterload as measured by peak systolic pressure and end systolic force-length relationship AND inotropic state (Which shifts the end systolic force-length relationship)

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13
Q

What happens to stroke volume if: end diastolic volume is kept constant and arterial pressure is decreased

A

increase

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14
Q

What happens to stroke volume if: load is kept constant and end diastolic volume is increased

A

increase

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15
Q

What happens to stroke volume if: arterial pressure increases,

A

decreases

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16
Q

What enables greater shortening form the same EDV against the same pressure?

A

increased inotropy

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17
Q

What two factors increase inotropy?

A

increased intrinsic heart rate, beta adrenergic input

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18
Q

What impairs inotropy?

A

metabolic abnormality

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19
Q

How is inotropy mediated?

A

calcium release

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20
Q

T/F LVEF is load/intropy independent

A

F

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21
Q

What happens to LVEF if: increase preload within limits

A

increase

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22
Q

What happens to LVEF if: increase afterload

A

decrease

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23
Q

What happens to LVEF if: decrease afterload

A

increase

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24
Q

What happens to LVEF if: increase inotropic state holding other variables constant

A

increase

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25
Q

_____ is determined by preload, afterload, and inotropic state.

A

stroke volume

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26
Q

_____ is determined by atrial pressure and ventricular diastolic dimension.

A

preload

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27
Q

_____ is determiend by arterial vascular resistance, cardiac output, and ventricular diastolic and systolic dimension.

A

afterload

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28
Q

_____ is determined by autonomic input to SA node.

A

heart rate

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29
Q

What provides the potential energy that drives systemic blood flow to all systemic tissues?

A

systemic arterial pressure

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30
Q

How do we calculate systemic vascular resistance/SVR?

A

mean arterial pressure/cardiac output = MAP/CO

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31
Q

What are the short term systemic arterial pressure sensors?

A

arterial/ventricular/atrial baroreceptors

32
Q

What are the long term systemic arterial pressure sensors?

A

renal baroreceptors

33
Q

Where are arterial baroreceptors located and how are they mediated?

A

carotid sinus and aortic arch –> cationic channels that respond to stretch

34
Q

What nerves are the afferents for arterial baroreceptors?

A

9 and 10

35
Q

What nerves are efferents component from arterial baroreceptors to heart and vessels?

A

sympa/parasympathetics

36
Q

What happens to the firing rate of arterial baroreceptors as they are stretched more?

A

increases

37
Q

What happens to the firing rate of arterial baroreceptors as they are stretched statically?

A

decays

38
Q

What do atrial baroreceptors sense?

A

atrial distension –> intravascular volume –> will release anp if too much iv volume to cause diuresis

39
Q

What do renal baroreceptors do?

A

release renin which leads to angiotensin production –> arterial vasoconstriction and retention of Na+ and H2O

40
Q

What happens to SA node rate? beta adrenergic stimulation

A

increase

41
Q

What happens to SA node rate? muscarinic stimulation

A

decrease

42
Q

What happens to AV node refractoriness and conduction velocity? beta adrenergic stimulation

A

reduced refract., increase conduction velocity

43
Q

What happens to AV node refractoriness and conduction velocity? muscarinic stimulation

A

increased refract., reduced conduction velocity

44
Q

What happens to the ventricles when stimulated by beta adrenergics?

A

increased inotropy

45
Q

What receptors mediate adrenergic vasoconstriction and in what tissues does this occur?

A

alpha adrenergic: renal, mesenteric, cutaneous

46
Q

What are the three natriuretic peptides?

A

atrial, btype, ctype

47
Q

What releases ANP and what is its function?

A

atria –> response to atrial stretch as in hypervolemia and exercise –> leads to increased GFR, reduced Na reabsorption, reduced renin secretion, increased smooth muscle relaxation

48
Q

What releases BNP and what is its function?

A

ventricles –> response to ventricular stretch –> similar actions as ANP

49
Q

What releases CNP and what is its function?

A

produced in vascular endothelium –> no diuretic activity, physiologic role less certain

50
Q

Adrenergic stimulation leads to venous constriction/dilation

A

constriction –> repartitions blood volume to central circulation, augments cardiac preload

51
Q

Muscarinic stimulation leads to venous constriction/dilation

A

dilation –> distributes blood into large veins, reduces cardiac preload

52
Q

What is the effect of gravitation/standing up on perfusion pressures?

A

upper body: lower pressure
lower body: higher pressure
*impaired venous return

53
Q

What is the effect of hemorrhage on systemic arterial pressure?

A

loss of iv volume causes loss of preload –> reduced cardiac output

54
Q

What is the fick cardiac output technique

A

measure CO by using oxygen as indicator –> CO = VO2/AVO2D = oxygen consumption/concentration difference is the arteriovenous oxygen difference

55
Q

What is thethermal dilution technique

A

catheter with tip thermistor positioned in main pulmonary artery –> colled by injected bolus of iced saline coming from right atrium –> CO calculated by integrating area under time termpreature curve –> small area = high CO, larg area = low CO

56
Q

What is normal mixed venous O2 sat?

A

75%

57
Q

A low CO will result in a low/high mixed O2 sat?

A

low

58
Q

Why does the reduction in diastolic filling time due to increased heart rate not reduce preload/stroke volume?

A

because most filling occurs during first 1/3 of diastole so high hear rates don’t really impair diastolic filling

59
Q

How do you overcome reduced ventricular ejection/stroke volume due to increase in afterload due to increased arterial pressure?

A

inotropic stimulation

60
Q

What is the pressure effect of increased local metabolic rate?

A

decrease local vascular resistance to match local flow to metabolic requirements –> reduced systemic vascular resistance –> decrease pressure

61
Q

inadequate blood flow to a tissue leading to metabolic derangement or cell necrosis

A

ischemia

62
Q

The majority of systemic vascular resistance occurs at the level of the _______

A

systemic arterioles

63
Q

Do medium sized arteries make an important contribution to vascular resistance?

A

no –> have flow-mediated vasodilation (endothelially regulated)

64
Q

Can blood get to venules without entering a capillary bed?

A

yes direct shunt between arteriole and venule

65
Q

What regulates arteriolar diameter?

A

tone of vascular smooth muscle

66
Q

Do vascular smooth muscle cells cycle between systole and diastole?

A

no –> but can exhibit chronic changes in basal tone –> controlled by cytosolic calcium concentration (increase calcium = increase basal tone)

67
Q

How is flow resistance related to arteriolar diameter?

A

r^4 –> subtle changes in arteriolar diameter can cause large changes in vascular resistance

68
Q

What is the difference between intrinsic and extrinsic control of VSMCs?

A

intrinsic control is based on the tissue’s local requirements whereas extrinsic control has to do with circulation’s overall requirements

69
Q

What are three effectors of intrinsic VSMC autoregulation?

A

myogenic autoregulation, endothelium mediated autoregulation, metabolic mediated autoregulation

70
Q

How does myogenic vascular autoregulation occur?

A

increase in arterial inflow pressure leads to increased SMC tone –> via stretch activated calcium channels (e.g. renal vascular bed)

71
Q

How does endothelium mediated vascular autoregulation occur?

A

increased endothelial shear stress –> activation of endothelial receptors –> NO release –> reduce SMC tone (mostly in distributing arteries vs. resistance vessels)

72
Q

How does metabolic mediated vascular autoregulation occur?

A

increased tissue metabolic activity leads to reduced SMC tone (possibly via adenosine)

73
Q

Resistance provided by vascular beds is effectively in series/parallel.

A

parallel –> different resistances determine the partitioning of blood flow

74
Q

What happens to systemic vascular resistance/SVR in: hypertension

A

disease process sets SVR to an abnormally high level leading to sustained elevation of systemic arterial pressure

75
Q

What happens to systemic vascular resistance/SVR in: CHF

A

normal homeostatic response to decreased CO increases SVR increases load on an already poorly functioning heart

76
Q

What happens to systemic vascular resistance/SVR in: sepsis

A

loss of normal SVR regulation mediated by circulating cytokines –> inappropriate opening of metarterioles (bypass capillaries), low systemic arterial pressure in setting of increased CO–> tissue ischemia in setting of increased blood flow

77
Q

What happens to systemic vascular resistance/SVR in: shock

A

low CO –> fall in systemic arterial pressure –> reduction in organ perfusion –> vasoconstriction of renal/cutaneous/GI beds to increase systemic vascular resistance –> restoration of systemic arterial pressure at the price of possible organ dysfunction (kidneys and liver)

Cardiology (41 decks)

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