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BRS Physio > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

Site of highest resistance in the cardiovascular system

A

arterioles

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2
Q

regulation of arterioles

A

ANS

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3
Q

Largest total cross-sectional and surface area

A

Capillaries

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4
Q

Contain the highest proportion of the blood

A

Veins

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5
Q

Velocity of blood flow equation

A

v = Q/A

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6
Q

Equation for Cardiac Output

A

Cardiac Output = (MAP-RAP)/(TPR)
MAP is mean arterial pressure
RAP is right atrial pressure
TPR is total peripheral resistance

CO = SV*HR

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7
Q

Poiseuille’s Equation

A

factors that change resistance of blood vessels
R = (8nl)/(pi*r^4)
n is viscosity of blood
l is length of blood vessel

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8
Q

Parallel resistance

A

1/R + 1/R + 1/R

when an artery is added in parallel, the total resistance decreases

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9
Q

Series Resistance

A

R = R+R+R
arrangement of BVs in an organ, total resistance is the sum of resistances
pressure decreases as it flows though a series of BV

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10
Q

Reynolds Number

A

predicts whether blood flow will be laminar or turbulent

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11
Q

Turbulent blood

A

high reynolds number, can cause bruits

decreased blood viscosity like anemia, increased blood velocity (narrowing of BV)

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12
Q

Capacitance

A

compliance, the distensibility of blood vessel
inversely related to elastance
C = (vol)/(pressure)

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13
Q

Mean Pressures in Systemic Circulation

A

Aorta - 100mmHg
Arterioles - 50mmHg
Capillaries - 20mmHg
Vena Cava - 4mmHg

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14
Q

Arterial Pressure

A

Systolic pressure is highest pressure

Diastolic pressure is lowest pressure

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15
Q

Most important determinant of pulse pressure

A

Stroke Volume

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16
Q

Eqtn for mean arterial pressure

A

DBP + 1/3 of pulse pressure

DBP + 1/3 (SBP-DBP)

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17
Q

Pulmonary Wedge Pressure

A

Estimates left atrial pressure

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18
Q

P wave

A

arterial depolarization

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19
Q

Decreased PR interval

A

increased conduction velocity through AV node (can be from sympathetic NS)

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20
Q

Increased PR interval

A

decreased conduction velocity through AV node (parasympathetic NS or heart block)

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21
Q

QRS complex

A

depolarization of the ventricles

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22
Q

QT interval

A

Beginning of Q wave to end of T wave

entire period of depolarization and repolarization of ventricles

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23
Q

PR interval

A

Initial depolarization of ventricle

beginning of P wave to beginning of Q wave

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24
Q

ST segment

A

isoelectric, period when ventricles are depolarized

from end of S wave to beginning of T wave

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25
Q

T wave

A

ventricular repolarization

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26
Q

Cardiac AP (Vent, Atria, Purkinje) - Phase 0

A

upstroke, from transient increase in Na conductance

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27
Q

Cardiac AP (Vent, Atria, Purkinje) - Phase 1

A

initial repolarization from outward current because of movement of K ions

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28
Q

Cardiac AP (Vent, Atria, Purkinje) - Phase 2

A

plateau of the AP
caused by transient increase in calcium conductance
inward calcium current by an increase in K conductance

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29
Q

Cardiac AP (Vent, Atria, Purkinje) - Phase 3

A

repolarization, K conductance predominates - large outward K current Ik

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30
Q

Cardiac AP (Vent, Atria, Purkinje) - Phase 4

A

RMP, period during which inward and outward currents Ik1 are equal

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31
Q

SA Node - Phase 0

A

upstroke AP, caused by increase in Calcium conductance

- increase causes an inward calcium current

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32
Q

SA Node - Phase 3

A

repolarization caused by an increase in K conductance - outward K current

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33
Q

SA Node - Phase 4

A

slow depolarization - inward Na current called If

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34
Q

Upstroke of AV node

A

Inward calcium current (like the SA Node)

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35
Q

Time required for excitation to spread throughout the cardiac tissue

A

Conduction Velocity

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36
Q

fastest conduction velocity in the heart

A

Purkinje system, slowest is AV node (PR interval)

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37
Q

Ability of cardiac cells to initiate APs in response to inward, depolarizing current

A

excitability

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38
Q

Effective refractory period

A

conducted AP cannot be elicited (cardiac)

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39
Q

decreases HR by decreasing the firing rate of SA node

A

Negative Chronotropic Effect

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40
Q

increases HR by increasing the firing rate of SA node

A 
Positive Chronotropic Effect
sympathetic effect (NE on B1)
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41
Q

decreases conduction velocity through the AV node, slowing the conduction of APs from atria to the ventricles

A

Negative dromotropic effect - increases PR interval

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42
Q

increases conduction velocity through the AV node, speeding the conduction of APs from atria to ventricles

A

Positive dromotropic effect - decreases PR interval

sympatehtic effect

43
Q

decreases HR by decreasing phase 4 depolarization

A

Negative chronotropic effect - parasympathetic on heart, decrease If

44
Q

decreases conduction velocity through AV node by decreasing inward calcium current and increase outward K current

A

Negative dromotrophic effect - parasympathetic on heart, increases PR interval

45
Q

Intercalated Disks

A

Cardiac Muscle that caontain gap junctions

46
Q

form dyads with SR

A

Cardiac T-tubules

47
Q

Inotropism

A

ability of heart to contract, related to intracellular calcium

48
Q

Positive staircase of Bowditch staircase

A

increased HR increases force of contraction in stepwise fashion as intracellular calcium increases

49
Q

Postextrasystolic potentiation

A

beat the occurs after an extrasystolic beat

50
Q

2 Mechanisms that increase force of contraction

A
  1. increases calcium current during plateau

2. increase calcium pump of SR by phosphorylated phospholamban thus increase calcium for release in subsequent beats

51
Q

Digitalis, cardiac glycosides

A

increase force of contraction by inhibiting Na/K-ATPase

which increases Calcium intracellularly

52
Q

Preload

A

end-diastolic volume which is related to Rt atrial pressure

53
Q

Afterload

A

for left ventricle - aortic pressure

for right ventricle - pulmonary artery pressure

54
Q

Maximal Velocity of contraction

A

when afterload is zero

55
Q

Frank-Starling

A

Increase in VR or EDV will cause an increase in SV and CO

56
Q

Increase Contractility will ____ cardiac output

A

increase

for any level of RAP or EDV

57
Q

Width of pressure-volume loop

A

Stroke Volume

58
Q

Increased preload on pressure-volume loop

A

causes an increase in stroke volume (width of graph gets bigger)
it is from increase EDV from increase VR

59
Q

Increased afterload on pressure-volume loop

A

causes a decrease in stroke volume (smaller width)
increases height of loop (thus skinnier and taller than normal)
due to increased aortic pressure

60
Q

Increased contractility on pressure-volume loop

A

causes an increase in SV (width gets bigger)
decrease in end-systolic volume
wider and taller pressure volume loop

61
Q

Stroke Volume

A

volume ejectied from the ventricle with each beat

SV = EDV-ESV

62
Q

Ejection Fraction

A

fraction of EDV ejected in each SV, related to contractility
normal is 55%
EF = SV/EDV

63
Q

Stroke Work

A

work the heart performs on each beat

aortic pressure)*(SV

64
Q

primary energy source for stroke work

A

Fatty Acids

65
Q

Cardiac Output by Fick Principle

A

CO = (O2 consumption)/(O2 in pulm v - O2 in pulm a)

66
Q

a wave on venous pulse curve

A

atrial systole

67
Q

4th heart sound

A

filling of ventricle by atrial systole (not audible in normal adults)

68
Q

begins after onset of QRS wave

A

isovolumetric ventricule contraction

69
Q

First heart sound

A

AV valve closes

70
Q

Split of 1st heart sound

A

because mitral valve closes before tricuspid valve

71
Q

2nd heart sound

A

Aortic Valve Closes

72
Q

3rd heart sound

A

rapid flow of blood from atria into ventricles

normal in children, not in adults

73
Q

Dicrotic notch or incisura

A

blip in aortic pressure tracing, occurs after closure of aortic valve

74
Q

Baroreceptor Reflex

A

stretch receptors in the carotid sinus near the bifurcation of common carotid arteries
decrease stretch leads to decrease firing rate of carotid sinus nerve (Hering, CN IX)
will decrease Parasymp and increase Sympathetics

75
Q

4 effects of AngII

A

1) stimulates the synthesis and secretion of aldosterone
2) increases Na/H-exchange to increase Na reabsorption
3) increase thirst
4) vasoconstriction of arterioles to increase TPR and arterial pressure

76
Q

Effects of Aldosterone

A

increase Na reabsorption in renal distal tubule to increase ECF and BV
slow process because needs to be synthesized first

77
Q

Cause for AngII release

A

decreased arterial pressure which causes decreased renal perfusion

78
Q

Cerebral Ischemia

A

pCO2 increases in brain

Chemoreceptors cause an increase in sympathetics to heart and BV

79
Q

Cushing reaction

A

response to cerebral ischemia

vasomotor center increases sympathetics outflow to heart and BV causing a profound increase in arterial pressure

80
Q

Chemoreceptors in carotid bodies and aortic arch

A

decrease in pO2 activate vasomotor centers producing vasoconstriction, increase in TPR and increase in arterial pressure

81
Q

ADH/Vasopressin

A

V1-receptors: on arterioles, a vasoconstrictor that increases TPR
V2-receptors: on distal tubules and collecting ducts, water reabsorption

82
Q

ANP

A

from atria in response to increased blood volume and atrial pressure
relaxes vascular smooth muscle, dilate arterioles
excretion of Na and water
inhibtis renin secretion

83
Q

How O2 and CO2 cross cell membranes

A

simple diffusion

84
Q

Starling equation

A 
Fluid flow = Kf[(Pc-Pi)-(osmc - osmi)]
fluid flow + it is net fluid out of capillary (filtration)
fluid flow (-) the net absorption
P means hydrostatic pressure
85
Q

factors that increase filtration

A

increase capillary hydrostatic pressure
decrease interstitial hydrostatic pressure
decrease protein concentration in capillaries
increase protein concentration in capillaries

86
Q

Organs that exhibit autoregulation

A

Heart, Brain, Kidney

blood flow remains constant over a wide range of perfusion pressures

87
Q

Active Hyperemia

A

blood flow to an organ is proportional to its metabolic activity
Ex is blood flow to skeletal muscle during exercise

88
Q

Reactive hyperemia

A

increase of blood flow to an organ that occurs after a period of occlusion of flow

89
Q

Myogenic Hypothesis

A

explains autoregulation of blood flow

vascular smooth muscle contracts when it is stretched

90
Q

Metabolic Hypothesis

A

tissue supply of oxygen is matched to the tissue demand for oxygen
vasodilators are produced:: CO2, H, K, lactate, and adenosine

91
Q

Histamine on Blood Vessels

A

arteriolar dilation and venous constriction

increase Pc to increase filtration

92
Q

bradykinin on blood vessels

A

arteriolar dilation and venous constriction

increase Pc to increase filtration

93
Q

Serotonin on blood vessels

A

Arteriolar constriction to prevent blood loss

implicated in vascular spasms of migraine headaches

94
Q

Prostaglandin E

A

vasodilator

95
Q

Prostaglandin F

A

vasoconstrictor

96
Q

Thromboxane A2

A

vasoconstrictor

97
Q

local metabolic factors in the coronary circulation

A

hypoxia and adenosine

98
Q

most important vasodilator for cerebral circulation

A

CO2

99
Q

Primary regulator of blood flow to skeletal muscle at rest

A

Sympathetic

  • alpha-1: vasoconstriction
  • Beta-2: vasodilation
100
Q

Local metabolites for skeletal muscle

A

lactate, adenosine, potassium

101
Q

Cardiovascular Changes when person is Standing

A

blood pools in veins, blood vol and VR decrease thus decreases SV and CO
Arterial pressure decreases
Compensatory mechanism: carotid sinus baroreceptors will increase sympathetics

102
Q

Cardiovascular Changes when person is Exercising

A

Sympathetics to heart and BV will increase
arteriolar resistance in the skin, splanchnic regions, kidneys and inactive muscles is increased
decrease TPR

103
Q

Cardiovascular Changes with hemorrhage

A

increase HR, contractility, TPR, cenoconstriction, renin, AngII, aldosterone, circulation NE and Epi, ADH

104
Q

Who gets locked out in their Penguin Footie Pajamas?

A

Jen-nay!!!

BRS Physio (7 decks)

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