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Physiology Modules 3-5 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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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
Veins have a a smaller lumen (T/F)
False - larger lumen and thinner walls - adventitia is thickest layer
26
Arteries have a high elastic content (T/F)
True to deal with pulsitile pressure
27
Thickest layer in arteries
Smooth muscle and connective tissue (muscularis)
28
Right AV valve is bi or tricuspid?
tricuspid
29
Left AV valve is bi or tricuspid?
bicuspid
30
Layers of heart wall (in to out)
endocardium, myocardium, epicardium, pericardium
31
Contractile myocardial cells interact with each other via
intercalated discs, gap junctions and desmosomes
32
An ECG positive wave means that the current is moving towards or away from the lead?
A depolarisation moving toward the lead or a re-polarisation moving away from the lead
33
An ECG negative wave means that the current is moving towards or away from the lead?
A depolarisation moving away from the lead
34
The QRS complex represents:
ventricular depolarisation
35
What is the nodal tissue??
The electrical cells - 1% (small round cells with little or no contractile tissue) Specialised for the generation and conduction of action potentials
36
What fraction of contractile cardiac cells contract per beat?
ALL of them!! just stronger or weaker sometimes
37
Speed of AP generation at SA node
100-110 beats/min | slowed by parasympathetic nerve
38
Speed of AP generation at AV node
0.05m/s | 5cm/s
39
AP conduction speed through atrial and ventricular myocardium
0.5m/s
40
Permeability to K+ is lower or higher in nodal cells compared to myocardial cells?
LOWER | Nodal cells let less permeable to K+ leading to an unstable and higher RMP of about -55 (compared to -70mV)
41
What are funny currents?
funny currents are the spontaneous initiation of action of the funny channels in nodal cells
42
How does a funny current occur?
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
Pacemaker potential
The slow depolarisation of the nodal cell from slow influx of Ca2+ between -60 and -40mV
44
Contractile cell AP process
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
Why can the heart not do tetanus/sustained contraction
longer absolute and relative refractory periods preventing re-excitation of the heart muscle
46
What are systole and diastole
contraction and relaxation
47
What happens in arrhythmias and atrial fibrillation?
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
What happens in ventricular fibrillation and defibrillation?
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
How full are the ventricles before the atria contract? (in%)
80-90%
50
Intrinsic Control of the heart
local controls originating entirely within the system | preload, afterload and contractility
51
Extrinsic Control of the heart
Hormonal, endocrine and nervous input
52
Stroke volume is? (definition and volume) | Explain SV = EDV - ESV
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
What is preload?
The amount of stretch/ filling of the heart before contraction Determined by the EDV and EDP: volume and pressure of ventricle before contraction
54
Frank - Starling mechanism
"More fill - more empty" | If ventricular volume increases, the heart responds by doing more work producing a larger stroke volume
55
Length - tension relationship
Short muscle - high overlap, generate small amount of contraction Stretched muscle - fibres cant overlap enough
56
Afterload
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
Catecholamine effect on the heart
Released from adrenal medulla and sympathetic nerves cause contraction and relaxation to occur more quickly Generate more force more quickly
58
Ejection Fraction equation
EJ = SV/EDV in mL | about 50 - 70%
59
Intrinsic mechanisms that control HR
Increase in right atrial pressure effects SA node | Increase in core temp by 1 degree increases HR by 10bpm
60
Effect of epinephrine on HR
Increase HR and SV
61
Law of Laplace
Muscle tension (which develops a ventricular pressure) depends on the radius of ventricle and thickness of ventricle wall
62
In law of laplace, what does a decrease in muscle wall thickness lead to?
increase in tension that needs to be generated (due to compliance of a thin wall compared to a thick wall)
63
What is the poiseuille relationship?
Laminar flow of a fluid is proportionally related to the radius, and the resistance
64
Pulse pressure is: | and is determined by:
the difference between systolic and diastolic pressure (120-80 = 40mmHg) Determined by: SV, speed of ejection, arterial compliance
65
arteriosclerosis
stiffening of the arteries (decrease in compliance)
66
Equation for blood flow:
Q = change in Pressure x Resistance
67
Which vessel type is important for adjusting TPR to maintain MABP?
arterioles
68
myogenic Regulation
stretching of the blood vessels, reaction is to constrict to prevent potential damage and maintain BP down the line
69
Sympathetic vasoconstricter nerves are controlled by and work how?
the brainstem, innervates most arterioles and veins and continue as varicosities which release dense-cored vesicles, containing noradrenaline and ATP
70
a- adrenoreceptors
cause vasocontriction Activated by noradrenaline, adrenaline and ATP tonically active
71
Reduced sympathetic activity results in: (vessels and actions)
vasodilation | Increased HR
72
Reduced sympathetic activity leads to: (vessels and actions)
vasoconstriction Increased TPR happens with blood loss
73
Vasodilater nerve neurotransmitter chemicals (3)
ACh - acetylcholine VIP - vasoactive intestinal peptide NO - nitric oxide
74
increased plasma epinephrine on arteioles
Increase vasoconstriction and dilation (skin) of the arterioles
75
increased plasma nor epinephrine on arteioles
Increase vasoconstriction of the arterioles
76
B2- adrenoreceptors
Causes vasodilation | Acted on by epinephrine/adrenaline
77
Vasoconstrictors
``` Adrenaline Noradrenaline ATP Angiotensin II Vasopressin (ADH) Endothelin O2 ```
78
Vasodilators
Adrenaline (skin B-receptors)) ACh, VIP and NO, PGI2, EDHF Atrial Natriuretic Peptide (ANP) Metabolites (CO2, lactate, H+, adenosine)
79
Myogenic autoregulation
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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