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Physiology Modules 3-5 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Hemodynamics

A

resistance, flow and pressure

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2
Q

Plasma is ?% of blood

A

55%

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3
Q

Circulation distributes (6) around the system

A

ions, water and CO2
heat
hormones
O2 and CO2

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4
Q

Blood circulation regulates (5)

A 
pH
Osmolarity
Body water
Temperature
Metabolism
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5
Q

Systemic and Pulmonary circuit are a …. circuit

A

Series

Get oxygen, deliver oxygen, repeat

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6
Q

Systemic circuit is arranged in a …… circuit

A

Parallel

Gives all organs their own blood flow

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7
Q

Approx stroke volume (mL)

A

70mL

60-80mL at rest

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8
Q

What is the stroke volume?

A

The amount of blood pumped out of each ventricle per beat

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9
Q

What is cardiac output?

A

The amount of blood pumped out of the heart per minute

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10
Q

Approx resting heart rate

A

70bpm

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11
Q

Approx cardiac output

A

5-6L/min

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12
Q

Equation for CO

A

CO = HR x SV

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13
Q

Blood flows from high to low pressure or low to high?

A

High to low

higher in the arteries than veins to keep pressure gradient and unidirectional flow

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14
Q

What does friction in the blood vessels cause?

A

Resistance to blood flow
Loss of energy from pumping
Drop in blood pressure

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15
Q

Blood flow determinants and equation

A

CHANGE IN PRESSURE from one part of the vessel to another (establish pressure gradient)
RESISTANCE to flow - from length, viscosity or radius of tube
F = (change in)P/R

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16
Q

Poiseuille’s Law

A

Tells us the 3 factors that govern resistance

  • Length of tube
  • Viscosity of liquid
  • Radius of tube (most impact in blood vessel resistance)
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17
Q

when we double the radius, the resistance increases by a factor of?

A

16
r^4 =1
2r^4 = 16

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18
Q

Where is most of the blood volume located?

A

Veins (40%)

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19
Q

How is cross sectional area and velocity of blood flow related

A

Smaller CSA = faster flow (e.g arteries)
Bigger CSA = slower flow (e.g. capillaries)
Speed and CSA like going from a river to the oean

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20
Q

What determines blood pressure gradient through vessels?

A

Highest pressure in arteries

Pulsitility needs to dampen before it reaches the capillaries

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21
Q

Primary function of aorta and large arteries

A

Receives highest pressure of blood and begins damping

- elastic and has to deal with high pulsitile pressure

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22
Q

Primary function of arteries and arterioles

A

resistance vessels which control the volume of flow through the circulation
- lots of smooth muscle to control radius and direction of blood flow

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23
Q

Primary function of capillaries

A

exchange of metabolites and O2

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24
Q

Primary function of venules and veins

A

return conduits, primary reservoir/capacitance of blood

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25
Q

Veins have a a smaller lumen (T/F)

A

False - larger lumen and thinner walls - adventitia is thickest layer

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26
Q

Arteries have a high elastic content (T/F)

A

True to deal with pulsitile pressure

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27
Q

Thickest layer in arteries

A

Smooth muscle and connective tissue (muscularis)

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28
Q

Right AV valve is bi or tricuspid?

A

tricuspid

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29
Q

Left AV valve is bi or tricuspid?

A

bicuspid

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30
Q

Layers of heart wall (in to out)

A

endocardium, myocardium, epicardium, pericardium

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31
Q

Contractile myocardial cells interact with each other via

A

intercalated discs, gap junctions and desmosomes

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32
Q

An ECG positive wave means that the current is moving towards or away from the lead?

A

A depolarisation moving toward the lead or a re-polarisation moving away from the lead

33
Q

An ECG negative wave means that the current is moving towards or away from the lead?

A

A depolarisation moving away from the lead

34
Q

The QRS complex represents:

A

ventricular depolarisation

35
Q

What is the nodal tissue??

A

The electrical cells - 1% (small round cells with little or no contractile tissue)
Specialised for the generation and conduction of action potentials

36
Q

What fraction of contractile cardiac cells contract per beat?

A

ALL of them!! just stronger or weaker sometimes

37
Q

Speed of AP generation at SA node

A

100-110 beats/min

slowed by parasympathetic nerve

38
Q

Speed of AP generation at AV node

A

0.05m/s

5cm/s

39
Q

AP conduction speed through atrial and ventricular myocardium

A

0.5m/s

40
Q

Permeability to K+ is lower or higher in nodal cells compared to myocardial cells?

A

LOWER

Nodal cells let less permeable to K+ leading to an unstable and higher RMP of about -55 (compared to -70mV)

41
Q

What are funny currents?

A

funny currents are the spontaneous initiation of action of the funny channels in nodal cells

42
Q

How does a funny current occur?

A

funny channels open and allows slow influx of Na+, depolarising the cell from -60mV to -40mV
At -40 the Ca2+ channels open and allow influx of Ca2+ up to +10mV when K+ channels open letting out K+ and re-polarising the cell back to 60mV

43
Q

Pacemaker potential

A

The slow depolarisation of the nodal cell from slow influx of Ca2+ between -60 and -40mV

44
Q

Contractile cell AP process

A

RMP = 90mV
Positive ions from neighbouring cell leak into the cell and depolarise it up to threshold of -70mV and then fast influx Na+ channels and slow influx Ca2+ channels open and lead to a fast depolarisation up to 0mV
Some K+ leaks out but is balanced by slow Ca2+ influx,

45
Q

Why can the heart not do tetanus/sustained contraction

A

longer absolute and relative refractory periods preventing re-excitation of the heart muscle

46
Q

What are systole and diastole

A

contraction and relaxation

47
Q

What happens in arrhythmias and atrial fibrillation?

A

Heart is shaky, SA node is no longer in control, uncoordinated contractions and the heart cant move blood properly, blood moving slower can cause stroke, treated with blood thinners (like aspirin and warfarin)

48
Q

What happens in ventricular fibrillation and defibrillation?

A

Is more life-threatening, ventricles pump without filling and if the rhythm is not rapidly reestablished (by defibrillation) then circulation stops and brain death occurs

  • almost no cardiac output
  • defib depolarises all the cells at the same time and hopes that they all repolarise together and the SA node can take over again
49
Q

How full are the ventricles before the atria contract? (in%)

A

80-90%

50
Q

Intrinsic Control of the heart

A

local controls originating entirely within the system

preload, afterload and contractility

51
Q

Extrinsic Control of the heart

A

Hormonal, endocrine and nervous input

52
Q

Stroke volume is? (definition and volume)

Explain SV = EDV - ESV

A

The amount of blood pumped out of the heart per contraction
65-70mL (60% of the blood in the ventricle)
End diastolic volume - End systolic volume, which is the volume before contraction - after

53
Q

What is preload?

A

The amount of stretch/ filling of the heart before contraction
Determined by the EDV and EDP: volume and pressure of ventricle before contraction

54
Q

Frank - Starling mechanism

A

“More fill - more empty”

If ventricular volume increases, the heart responds by doing more work producing a larger stroke volume

55
Q

Length - tension relationship

A

Short muscle - high overlap, generate small amount of contraction
Stretched muscle - fibres cant overlap enough

56
Q

Afterload

A

The tension the fibres must generate before they can shorten
The pressure that the ventricles must overcome to force open the semilunar valves
Afterload can increase from hypertension

57
Q

Catecholamine effect on the heart

A

Released from adrenal medulla and sympathetic nerves cause contraction and relaxation to occur more quickly
Generate more force more quickly

58
Q

Ejection Fraction equation

A

EJ = SV/EDV in mL

about 50 - 70%

59
Q

Intrinsic mechanisms that control HR

A

Increase in right atrial pressure effects SA node

Increase in core temp by 1 degree increases HR by 10bpm

60
Q

Effect of epinephrine on HR

A

Increase HR and SV

61
Q

Law of Laplace

A

Muscle tension (which develops a ventricular pressure) depends on the radius of ventricle and thickness of ventricle wall

62
Q

In law of laplace, what does a decrease in muscle wall thickness lead to?

A

increase in tension that needs to be generated (due to compliance of a thin wall compared to a thick wall)

63
Q

What is the poiseuille relationship?

A

Laminar flow of a fluid is proportionally related to the radius, and the resistance

64
Q

Pulse pressure is:

and is determined by:

A

the difference between systolic and diastolic pressure (120-80 = 40mmHg)
Determined by: SV, speed of ejection, arterial compliance

65
Q

arteriosclerosis

A

stiffening of the arteries (decrease in compliance)

66
Q

Equation for blood flow:

A

Q = change in Pressure x Resistance

67
Q

Which vessel type is important for adjusting TPR to maintain MABP?

A

arterioles

68
Q

myogenic Regulation

A

stretching of the blood vessels, reaction is to constrict to prevent potential damage and maintain BP down the line

69
Q

Sympathetic vasoconstricter nerves are controlled by and work how?

A

the brainstem, innervates most arterioles and veins and continue as varicosities which release dense-cored vesicles, containing noradrenaline and ATP

70
Q

a- adrenoreceptors

A

cause vasocontriction
Activated by noradrenaline, adrenaline and ATP
tonically active

71
Q

Reduced sympathetic activity results in: (vessels and actions)

A

vasodilation

Increased HR

72
Q

Reduced sympathetic activity leads to: (vessels and actions)

A

vasoconstriction
Increased TPR
happens with blood loss

73
Q

Vasodilater nerve neurotransmitter chemicals (3)

A

ACh - acetylcholine
VIP - vasoactive intestinal peptide
NO - nitric oxide

74
Q

increased plasma epinephrine on arteioles

A

Increase vasoconstriction and dilation (skin) of the arterioles

75
Q

increased plasma nor epinephrine on arteioles

A

Increase vasoconstriction of the arterioles

76
Q

B2- adrenoreceptors

A

Causes vasodilation

Acted on by epinephrine/adrenaline

77
Q

Vasoconstrictors

A 
Adrenaline
Noradrenaline
ATP
Angiotensin II
Vasopressin (ADH)
Endothelin
O2
78
Q

Vasodilators

A

Adrenaline (skin B-receptors))
ACh, VIP and NO, PGI2, EDHF
Atrial Natriuretic Peptide (ANP)
Metabolites (CO2, lactate, H+, adenosine)

79
Q

Myogenic autoregulation

A

Myogenic/autoregulation when resistance vessels detect and respond directly to and in/decrease in pressure by vasodilation or constriction
When pressure decreases, the vessels dilate to decrease TPR and increase flow
- goal is to keep flow relatively the same

Physiology Modules 3-5 (7 decks)

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