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N542 Physiology > CV > Flashcards

CV Flashcards

0
Q

Why is the plateau in the action potential of the cardiac cell important to its function?

A

It allows for filling of the atria and ventricles and contraction of the muscle

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1
Q

How does the action potential differ from cardiac and skeletal muscle?

A

Cardiac has a plateau caused by slow Ca channels opening AND immediate decrease in K permeability, causing slower repolarization back to resting potential, also Na channels that start the potential are slightly slower in cardiac cells
The plateau is 0.2 sec long, 15x longer than skeletal muscle action potential

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2
Q

How does excitation-contraction coupling differ between skeletal and cardiac cells?

A

SR of cardiac cells isn’t as developed as skeletal cells, so cardiac cells rely on Ca entering from EXTRACELLULAR T-tubules for the strength of contraction (in skeletal cells, the strength relies on INTRACELLULAR Ca from SR)
Also, T-tubules are 5x the size in cardiac cells

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3
Q

Absolute vs. Relative Refractory period

A

Absolute: another action potential can’t occur at this time
Relative: another action potential can occur, PVCs/PACs happen at this time

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4
Q

Why is the SA node responsible for the HR?

A

SA node fibers have ability for “self-excitation”, this is caused by leaking Na channels which give the SA node a higher resting potential than ventricular fibers

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5
Q

What is the significance of the delay of impulse from SA to AV node, how long is the delay?

A

Delay is caused by less gap junctions which increases resistance of impulse, decreasing speed of impulse by 0.16 sec
This delay allows time for atria to empty into the ventricles before ventricular contraction, contributing to 20% of stroke volume

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6
Q

In the cardiac cycle, when does the AV valve open and close?

A

Opens at the end of isovolumetric relaxation, when it opens, the period of filling begins
Closes at the end of filling (after atrial kick), when it closes, isovolumetric contraction begins

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7
Q

When does the aortic valve open and close in the cardiac cycle?

A

Opens after isovolumetric contraction, then period of ejection occurs
Closes after period of ejection, then isovolumetric relaxation occurs

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8
Q

Pressure in RA, RV, RV end diastolic pressure, and PA

A

RA 9/4 (mean 5)
RV 25/4
RV end diastolic <6
PA 25/15

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9
Q

Pressure in LA, LV, LV end diastolic and Aortic pressure

Which of these values is a wedge pressure?

A

LA (wedge) 12/5 (mean 9)
LV 120/4
LV end diastolic pressure <12
Aorta (ABP) 120/80

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10
Q

What are O2 sats on R side of heart vs. L side of heart

A

R: 75%
L: 95%

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11
Q

How do you calculate stroke volume using the pressure volume loop?

A

SV = EDV-ESV

end diastolic volume - end systolic volume

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12
Q

How do you calculate ejection fraction?

A

SV / EDV
(stroke volume/end diastolic volume)
The proportion of volume ejected during systole

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13
Q

Where in the pressure-volume loop is preload measured and what is it affected by?

A

Measured at end diastolic pressure/volume period (when ventricles are full)
Affected by venous tone and blood volume (aka. venous pressure and venous return)
(Book definition: degree of tension on the muscle when it begins to contract)

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14
Q

Where in the pressure-volume loop is afterload measured and what is it affected by?

A

Pressure during ejection
(Book definition: the load against which the muscle exerts contractile force)
Affected by pressure in aorta leaving from the ventricle

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15
Q

During exercise, how much can cardiac output increase?

A

4-7x the amount

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16
Q

Frank Starling Law

A

The heart will pump out the volume that comes in
The greater the stretch during filling, the greater the force of contraction and the greater the quantity of blood pumped into the aorta

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17
Q

How does the sympathetic and parasympathetic innervation affect the heart?

A

Sympathetic: increase HR (B1) and contractility (A1, B1)
Parasympathetic: decreases HR slightly

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18
Q

What does max sympathetic stimulation do to cardiac output? What are some examples?

A

It doubles cardiac output

Ex: drugs like cocaine, intubating

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19
Q

Excess K extracellular does what to the cardiac cell?

A

Dilates myocardium
Decreases HR and decreases INTENSITY of action potential and contraction
In the action potential, resting potential is depolarized more than normal, the potential doesn’t go very far to reach threshold (NET change is less), so response is lessened

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20
Q

Excess Ca in extracellular does what to cardiac cells?

A

Causes spastic contraction

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21
Q

What percent of blood is in the veins? What percent is in the heart? Lungs?

A

Veins: 60%
Heart: 7%
Lungs: 9%

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22
Q

How does the cardiac output differ between the R and L ventricles?

A

They are the SAME

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23
Q

How do pulmonary and systemic circulation differ?

A

Systemic is high resistance and high pressure, this is a parallel circuit
Pulmonary is low pressure, low resistance (low velocity)

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24
Q

Where in the circulation is the largest pulse pressure?

A

LV (120/4)

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25
Q

Factors that influence systolic and diastolic pressure?

A

Aortic distensibility (stiffness), stroke volume, heart rate, peripheral resistance, ejection velocity

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26
Q

What equation is used to determine blood flow through a vessel using only pressure and resistance?

A

Ohm’s law
Flow = change in pressure / resistance
Therefore, flow is directly related to pressure and inversely related to resistance

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27
Q

How is it determined if blood flow is laminar or turbulent?

A

Reynold’s number = density x diameter x velocity / viscosity

2000+ is turbulent

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28
Q

What is turbulent flow

A

Blood flow is too fast that it spirals in all direction, it can be caused by blood passing a rough surface (plaque) or obstruction
Turbulent flow causes blood to flow with more resistance and friction

29
Q

What equation determines flow using viscosity and length of the tube? This equation shows that the radius of a tube is the most important factor determining flow.

A

Poiseuille’s Law

Flow = (pi x pressure change x r^4) / (8 x viscosity x length)

30
Q

What is the relationship of the total resistance to all the resistances of the vessels in parallel? How can this be applied to removing a limb/organ?

A

1/Rtotal = 1/R1 + 1/R2 …
More blood will flow through the whole parallel system than one vessel, so the total resistance is less than the resistance in one vessel
Taking away flow (decreasing conductance) to an organ/limb will increase total peripheral vascular resistance

31
Q

What equation is used to determine capillary flow? What causes edema?

A

Laplace’s law, T = P x r
tension = pressure x radius
Increased pressure causes slits to be made in the capillary, leaking, and edema, (wall stress)

32
Q

What can endothelial cells release that vasodilate and vasoconstrict?

A

NO is released because of stress on the endothelial cells, it causes vasodilation
Endothelin is released when a blood vessel is injured, it causes vasoconstriction

33
Q

Metabolic theory of autoregulation

A

when BP increases, there is too much oxygen to the tissue it “washes out” the vasodilators, thus causing vasocontriction
when BP decreases, the decrease in oxygen to the tissue allows vasodilator substances to get released, causing more flow and oxygen to the tissue

34
Q

What are the specific vasodilators released in the metabolic theory

A

adenosine, carbon dioxide (especially in the brain, to decrease ICP), ATP/ADP compounds, histamine, K (and Mg), and H ions

35
Q

What is the myogenic theory of autoregulation?

A

the stretch of small blood vessels (vascular smooth muscle) causes constriction to keep the flow of blood constant

36
Q

Endothelial cells can release nitric oxide and endothelin, what do these do?

A

NO causes vasodilation (it is released from stress on the endothelial cells)
Endothelin causes vasoconstriction (it is released when a blood vessel is injured)

37
Q

What organ is not involved in the metabolic theory (vasodilation is NOT occuring in this organ in response to low oxygen)

A

The lungs, in order to get more oxygen to this area, pulmonary vasoconstriction must occur

38
Q

Angiogenesis

A

Over time, if there is an increased metabolic need to an area (causes: plaque build up, altitude/oxygen), collateral circulation will start to be built to perfuse the tissues appropriately
This is done by VEGF (vasc. endothelin growth factor), Fibroblast growth factor, and angiogenin

39
Q

Where is the neurogenic vasoconstrictor area of the brain located?

A

Bilaterally in the anterolateral portion of the upper medulla, preganglionic neurons extend to spinal cord

40
Q

Where is the neurogenic vasodilator area of the brain?

A

Bilateral anterolateral portion of the lower medulla, these fibers reach up and inhibit the vasoconstrictor activity in the upper medulla

41
Q

How does the neurogenic control work to provide “reflexes” (ex: baroreceptor reflex)? What structures does it pass through?

A

Neurons get sensory signals from the vagus and glossopharyngeal nerves. Sensory area is bilaterally in tractus solitarius in posterolateral portions of medulla and lower pons. Then the impulse travels out to control vasoconstrictor and vasodilator centers, providing reflex control of circulatory functions.

42
Q

What causes vasomotor tone?

A

Repeated impulses maintaining a partial state of contraction in the vessel

43
Q

Lateral vasomotor center vs. Medial vasomotor center impulses?

A

Lateral excites SNS to increase HR and increase contractility
Medial signals dorsal motor nuclei of vagus nerves to decrease HR and decrease contractility

44
Q

Baroreceptor reflex

A

Stretch is detected by a baroreceptor, then a signal is transmitted to CNS saying that there is a raise in pressure, so feedback signals are sent back to decrease pressure by slowing the heart down
“as BP increases, HR decreases”

45
Q

Bainbridge reflex

A

Stretch in the atria (increased volume) initiates this reflex through vagus nerves, response is increased HR and increased contractility (prevents pooling of the blood)
Note: even though the vagus nerves are involved in this reflex, the HR increases because the vagus does not overpower SNS response

46
Q

Normal cardiac output of average males vs. females

A

male: 5.5 L/min
female: 5 L/min

47
Q

Cardiac Index: how is it measured and what is the average value

A

CO related to body size
CO/BSA in m^2
For 170lb person, 5L/min/1.5m^2 = 3.3 L/min/m^2

48
Q

What equations related cardiac output to HR, SV, SVR, and arterial pressure? And what is the fick principle?

A 
CO = HR x SV this equation uses fick principle, determines how much does the heart use and how much it leaves behind
CO = arterial pressure / SVR
49
Q

How does arterial pressure change with inspiration?

A

Pressure in the thoracic cavity becomes more negative, causes blood vessels in the chest to expand, decreases blood the left side of the heart, decreases CO, decreases ABP

50
Q

What factors decrease cardiac output?

A

decreased blood volume, venous dilation (SNS inactive, blood “pools”), venous obstruction, decreased tissue/skeletal muscle mass, decreased metabolic rate of tissue (ex. bedrest, hypothyroid)

51
Q

factors that increase RA pressure (impacting cardiac output)

A

PPV (pos pressure ventilation), opening of thoracic cage, cardiac tamponade

52
Q

What factors effect venous return? What equation is used?

A

RA pressure, degree of filling (filling pressure), and resistance to blood flow (mostly venous)
VR = (Psf - PRA) / RVR
venous return = mean systemic filling - RA pressure / resistance to venous return
Normal: 5L/min = 7-0 mmHg / 1.4mmHg/L/min

53
Q

What percent (and how many mL/min) of cardiac output goes to coronary flow?

A

5% (225-250mL/min)

54
Q

What does the L coronary artery supply?

A

anterior and L lateral portion of L ventricle

55
Q

What does R coronary artery supply?

A

R ventricle and posterior of L ventricle

56
Q

Increased preload has what effect on stroke volume and EDV

A

increases stroke volume and increases EDV

57
Q

Increased afterload has what effect on stroke volume and ESV

A

decreases stroke volume and increases ESV

58
Q

Increased inotropy has what effect on stroke volume and ESV?

A

Increases stroke volume, decreases ESV

59
Q

Where are baroreceptors found and what are the parasympathetic innervations?

A

Carotid sinus and aortic arch
Carotid: Glossopharyngeal
Aortic: Vagus

60
Q

What factors can lead to increased preload (ventricular filling)?

A

decreased HR, increased atrial contractility, increased ventricular compliance, increased aortic pressure, increased CVP (decreased venous compliance: ex. PVD, stiff valves, increased thoracic venous blood volume)

61
Q

What factors increase inotropy?

A

Circulating catecholamines, HR, afterload, SNS activation, PSNS inhibition

62
Q

Stroke work, definition and equation

A

SW = SV x MAP

work done by the ventricle to eject the volume of blood into the aorta (against the pressure in the aorta)

63
Q

MAP equation

A

diastolic arterial pressure + 1/3 arterial pulse pressure

64
Q

Systemic circulation vs. Regional circulation

A

Systemic: circulation to all the body EXCEPT the pulmonary circuit, originating the L ventricle
Regional: circulation to a specific organ within systemic circulation

65
Q

Which vessel has the greatest resistance to flow?

A

arterioles

66
Q

How does resistance compare to radius of a vessel?

A

Resistance is INVERSELY related to radius to the fourth power

67
Q

What vessel has the highest total cross sectional area?

A

capillaries

68
Q

Which organs are greedy in that they have high % of blood flow to the organ and low VO2 (high O2 consumption)?

A

Kidney (22% blood flow) and brain (15% blood flow)

69
Q

What is the normal VO2 (oxygen consumption/metabolism) of the heart?

A

250 mL O2/ min

70
Q

Which fibers have the greatest velocity.. SA, AV, purkinje?

A

purkinje

N542 Physiology (9 decks)

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