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

Question 1

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

Answer 1

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

Question 2

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

Answer 2

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

Question 3

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

Answer 3

subendocardial myocytes shorten more than the epicardial surface

Question 4

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

Answer 4

Ventricular afterload

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

At what point is systolic wall stress greatest?

Answer 7

at onset of ejection as ventricular volume is largest

Question 8

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

Answer 8

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

Question 9

What is the increased inotropic state of cardiac muscle?

Answer 9

cardiac muscle can increase force at any given length

Question 10

What determines ventricular stroke volume?

Answer 10

EDV-ESV

Question 11

What determines EDV?

Answer 11

preload as measured by EDP and diastolic force-length relationship

Question 12

What determines ESV?

Answer 12

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

Question 13

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

Answer 13

increase

Question 14

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

Answer 14

increase

Question 15

What happens to stroke volume if: arterial pressure increases,

Answer 15

decreases

Question 16

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

Answer 16

increased inotropy

Question 17

What two factors increase inotropy?

Answer 17

increased intrinsic heart rate, beta adrenergic input

Question 18

What impairs inotropy?

Answer 18

metabolic abnormality

Question 19

How is inotropy mediated?

Answer 19

calcium release

Question 20

T/F LVEF is load/intropy independent

Answer 20

F

Question 21

What happens to LVEF if: increase preload within limits

Answer 21

increase

Question 22

What happens to LVEF if: increase afterload

Answer 22

decrease

Question 23

What happens to LVEF if: decrease afterload

Answer 23

increase

Question 24

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

Answer 24

increase

Question 25

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

Answer 25

stroke volume

Question 26

_____ is determined by atrial pressure and ventricular diastolic dimension.

Answer 26

preload

Question 27

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

Answer 27

afterload

Question 28

_____ is determined by autonomic input to SA node.

Answer 28

heart rate

Question 29

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

Answer 29

systemic arterial pressure

Question 30

How do we calculate systemic vascular resistance/SVR?

Answer 30

mean arterial pressure/cardiac output = MAP/CO

Question 31

What are the short term systemic arterial pressure sensors?

Answer 31

arterial/ventricular/atrial baroreceptors

Question 32

What are the long term systemic arterial pressure sensors?

Answer 32

renal baroreceptors

Question 33

Where are arterial baroreceptors located and how are they mediated?

Answer 33

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

Question 34

What nerves are the afferents for arterial baroreceptors?

Answer 34

9 and 10

Question 35

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

Answer 35

sympa/parasympathetics

Question 36

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

Answer 36

increases

Question 37

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

Answer 37

decays

Question 38

What do atrial baroreceptors sense?

Answer 38

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

Question 39

What do renal baroreceptors do?

Answer 39

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

Question 40

What happens to SA node rate? beta adrenergic stimulation

Answer 40

increase

Question 41

What happens to SA node rate? muscarinic stimulation

Answer 41

decrease

Question 42

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

Answer 42

reduced refract., increase conduction velocity

Question 43

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

Answer 43

increased refract., reduced conduction velocity

Question 44

What happens to the ventricles when stimulated by beta adrenergics?

Answer 44

increased inotropy

Question 45

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

Answer 45

alpha adrenergic: renal, mesenteric, cutaneous

Question 46

What are the three natriuretic peptides?

Answer 46

atrial, btype, ctype

Question 47

What releases ANP and what is its function?

Answer 47

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

Question 48

What releases BNP and what is its function?

Answer 48

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

Question 49

What releases CNP and what is its function?

Answer 49

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

Question 50

Adrenergic stimulation leads to venous constriction/dilation

Answer 50

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

Question 51

Muscarinic stimulation leads to venous constriction/dilation

Answer 51

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

Question 52

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

Answer 52

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

Question 53

What is the effect of hemorrhage on systemic arterial pressure?

Answer 53

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

Question 54

What is the fick cardiac output technique

Answer 54

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

Question 55

What is thethermal dilution technique

Answer 55

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

Question 56

What is normal mixed venous O2 sat?

Answer 56

75%

Question 57

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

Answer 57

low

Question 58

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

Answer 58

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

Question 59

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

Answer 59

inotropic stimulation

Question 60

What is the pressure effect of increased local metabolic rate?

Answer 60

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

Question 61

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

Answer 61

ischemia

Question 62

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

Answer 62

systemic arterioles

Question 63

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

Answer 63

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

Question 64

Can blood get to venules without entering a capillary bed?

Answer 64

yes direct shunt between arteriole and venule

Question 65

What regulates arteriolar diameter?

Answer 65

tone of vascular smooth muscle

Question 66

Do vascular smooth muscle cells cycle between systole and diastole?

Answer 66

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

Question 67

How is flow resistance related to arteriolar diameter?

Answer 67

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

Question 68

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

Answer 68

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

Question 69

What are three effectors of intrinsic VSMC autoregulation?

Answer 69

myogenic autoregulation, endothelium mediated autoregulation, metabolic mediated autoregulation

Question 70

How does myogenic vascular autoregulation occur?

Answer 70

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

Question 71

How does endothelium mediated vascular autoregulation occur?

Answer 71

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

Question 72

How does metabolic mediated vascular autoregulation occur?

Answer 72

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

Question 73

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

Answer 73

parallel --> different resistances determine the partitioning of blood flow

Question 74

What happens to systemic vascular resistance/SVR in: hypertension

Answer 74

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

Question 75

What happens to systemic vascular resistance/SVR in: CHF

Answer 75

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

Question 76

What happens to systemic vascular resistance/SVR in: sepsis

Answer 76

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

Question 77

What happens to systemic vascular resistance/SVR in: shock

Answer 77

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)