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Physio Exam 2 > Ziolo Lectures > Flashcards

Ziolo Lectures Flashcards

1
Q

The hematocrit is a

A

rapid assessment of blood composition.It is the percent of the blood volume that is composed of RBCs (red blood cells).

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2
Q

Buffy coat is negligible when calculating

A

hematocrit

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3
Q

Arterioles+capillaries+venules=

A

microcirculation

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4
Q

Flow =

A

volume per unit time

F= ΔP/R

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5
Q

Resistance is roughly

A

1/radius^4

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6
Q

Blood viscosity can

A

alter

resistance and thereby flow.

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7
Q

Main function of valves –

A

isolate electrically atria from ventricle.

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8
Q

cardiac muscle isElectrically coupled through

A

gap junctions located in intercalated disc.

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9
Q

Parasympathetic releases ——— to

A

acetylcholine to muscarinic receptors

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10
Q

Sympathetic releases ——— to

A

norepinephrine/epinephrine, Beta = beta adronergic receptors.

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11
Q

Both nodes can

A

spontaneously depolarize – SA does this faster.

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12
Q

Bundle of His

A

depolarizes slower than AV node.

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13
Q

The rapid opening of voltage-gated sodium channels is responsible for

A

the rapid depolarization phase.

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14
Q

The prolonged “plateau” of

depolarization is due to the

A 
slow 
but prolonged opening of 
voltage-gated calcium channels 
          PLUS
closure of potassium channels
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15
Q

Calcium influx doesn’t allow for

A

repolarizing. Longer refractory period.

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16
Q

Opening of potassium

channels results in the

A

repolarization phase.

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17
Q

Sodium ions can “leak” in through

the

A

F-type [funny] channels

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18
Q

calcium ions

A

can move in through
the T [calcium] channels cause a
threshold graded depolarization.

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19
Q

The rapid opening of voltage-gated
calcium channels is responsible
for the

A

rapid depolarization phase

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20
Q

Reopening of potassium channels
PLUS
closing of calcium channels
are responsible for the

A

repolarization phase.

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21
Q

Excitation-Contraction Coupling links the

A

cardiac muscle cell action potentials

to contraction via control of calcium within the myocardium.

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22
Q

First heart sound –

A

closure of the AV valves

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23
Q

Second heart sound –

A

closure of the aortic and pulmonary valves

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24
Q

Murmurs

A

stenosis

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25
Q

Stenosis =

A

narrowing

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26
Q

Regurgitation =

A

insufficiency

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27
Q

Systole:

A

ventricles contracting

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28
Q

Diastole:

A

ventricles relaxed

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29
Q

Cardiac output (CO) =

A

Heart rate (HR) x Stroke volume (SV)

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30
Q

Atria influences

A

HR,

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31
Q

ventricles influence

A

stroke volume.

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32
Q

PS only decreases

A

HR.

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33
Q

To speed up the heart rate:

A

deliver the sympathetic hormone, epinephrine, and/or
release more sympathetic neurotransmitter (norepinephrine), and/or
reduce release of parasympathetic neurotransmitter (acetylcholine).

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34
Q

Preload –

A

the volume of blood in the ventricles just before contraction. End-diastolic volume

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35
Q

Afterload –

A

the pressure against which the ventricle pumps

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36
Q

To increase the heart’s stroke volume:

A

fill it more fully with blood. The increased stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap.

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37
Q

To further increase the stroke volume:
fill it more fully with blood AND
deliver

A 
sympathetic signals (norepinephrine and epinephrine);
	it will also relax more rapidly, allowing more time to refill
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38
Q

Sympathetic signals (norepinephrine and epinephrine) cause a

A

stronger and more rapid contraction and a more rapid relaxation.

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39
Q

To increase SV, increase:

A 
end-diastolic volume, norepinephrine 
delivery from sympathetic 
neurons, and
epinephrine 
delivery 
from the 
adrenal 
medulla
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40
Q

To increase HR, increase:

A 
norepinephrine delivery from 
sympathetic neurons, and
epinephrine 
delivery from 
adrenal medulla
(reduce 
parasympathetic).
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41
Q

Thermodilution Cardiac Output

is a

A

measurement of cardiac function

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42
Q

Ejection fraction =

A

measurement of contractility. Defined as the ratio of the stroke volume (end diastolic volume [EDV] minus end systolic volume [ESV]) to the end-diastolic volume
EDV-ESV/EDV.

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43
Q

Hypertrophic cardiomyopathy is

A

preload dependent

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44
Q

Arterioles can adjust

A

diameter to regulate blood flow.

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45
Q

In response to the pulsatile contraction of the heart:

pulses of pressure move throughout the vasculature, decreasing in

A

amplitude with distance

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46
Q

Compliance =

A

Δ volume/Δ pressure

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47
Q

Veins and venules have highest .

A

compliance

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48
Q

Maximum arterial pressure =

A

systolic pressure (SP)

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49
Q

Minimum arterial pressure =

A

diastolic pressure (DP)

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50
Q

Pulse pressure =

A

SP – DP

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51
Q

Pulse pressure isDetermined by:

A

stoke volume
Speed of ejection of the stroke volume
Arterial compliance

52
Q

Mean arterial pressure =

A

DP + 1/3(SP-DP)

53
Q

MAP =

A

pressure driving blood into the tissues

averaged over the cardiac cycle

54
Q

Arterioles

A

Determine the relative blood flow to that organ

In composite determine the mean arterial pressure

55
Q

Forgan=

A

(MAP- venous pressure)/Resistanceorgan

because venous pressure is close to) 0 mmHg

56
Q

Forgan=

A

MAP/Resistanceorgan

57
Q

Dynamic adjustments in the blood distribution to the

organs is accomplished by

A

relaxation and contraction

of circular smooth muscle in the arterioles.

58
Q

Arteriole Intrinsic tone

Controlled by:

A

Local controls

Extrinsic controls

59
Q

Active hyperemia and flow autoregulation differ in their

cause but both result

A

in the production of the same

local signals that provoke vasodilation.

60
Q 
Local controls
(arteriole intrinsic tone)
A

Active hyperemia

Flow autoregulation

61
Q

Active hyperemia:

A

** accumulation of: CO2, H+, K+, eicosanoids, adenosine, bradykinin, nitric oxide (NO)

62
Q

Flow autoregulation:

A
    • myogenic responses – some arteriolar smooth muscle respond to increased stretch caused by increased pressure by contracting to a greater extent (Converse is also true).
      • Reactive hyperemia – response to cessation of blood flow
63
Q

Sympathetic stimulation of alpha-adrenergic receptors causes

A

vasoconstriction to decrease blood flow to that location.

64
Q

Sympathetic stimulation of beta-adrenergic receptors leads to

A

vasodilation to cause an increase in blood flow to that location.

65
Q

Endothelial controls: Arterioles:

A

Paracrine effect:

Flow induced arterial vasodilation

66
Q

Paracrine effect:

A 
Vasodilators:
-Endothelium derived relaxing factor (EDRF) = Nitric oxide (NO)
-Prostacyclin (PGI2)
Vasoconstrictor
-Endothelin-1
67
Q

Diversity among signals that influence contraction/relaxation
in vascular circular smooth muscle implies a diversity of

A

receptors and transduction mechanisms.

68
Q

Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream metarterioles and precapillary sphincters determine the

A

volume of blood each capillary receives

69
Q

Low molecular weight penetrating solutes =

A

crytalloids

70
Q

Non-penetrating plasma proteins =

A

colloids

71
Q

PC=

A

capillary hydrostatic pressure (favoring fluid movement out of the capillary

72
Q

PIF=

A

Interstitial hydrostatic pressure (favoring fluid movement into the capillary)

73
Q

πC=

A

Osmotic force due to plasma protein concentration (favoring movement into the capillary)

74
Q

πIF=

A

Osmotic force due to interstitial fluid protein concentration (favoring movement out of the capillary

75
Q

At rest, approx.

A

60% of the total blood volume is in the veins.

76
Q

Sympathetically mediated venoconstriction can substantially

A

increase venous return to the heart.

77
Q

Alterations in “venous return” alter

A

end-diastolic volume (EDV);

78
Q

increased EDV directly increases

A

stroke volume and cardiac output.

79
Q

vFerritin serves as a storage buffer for

A

iron

80
Q

RBC life span ~

A

120 days, 1% of RBC replaced daily (~250 billion RBC)

81
Q

Iron released from destroyed RBC is bound by

A

transferrin and delivered to bone marrow.

82
Q

Erythropoiesis is

hormonally regulated:

A

decreased oxygen delivery to the kidney causes the secretion of erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis.

83
Q

Anemia: Decrease in the ability of the blood to

A

carry oxygen
due to:
- decrease in the total number of erythrocytes
- diminished concentation of hemoglobin
- combination

84
Q

Collagen is a

A

“magnet for platelets,”

which then become one of the sources of signals that alter blood flow and initiate the steps of clot formation at the affected site
85
Q

Thrombin IX loss results in

A

Genetic absence results in hemophilia

excessive bleeding

86
Q

*Clotting can occur in the absence of all

cellular elements except

A

platelets***

87
Q

Delta P, which is called the perfusion pressure, is the same for all

A

vascular beds; it is equal to MAP–VP, (VP is venous pressure)

88
Q

Because blood flows along the path of

A

least resistance, organs with the lowest resistance will receive the highest flow.

89
Q

Most of the decrease in resistance will be in the

A

arterioles. They have the most smooth muscle and they also have the largest resistance.

90
Q

Mean systemic arterial pressure is the product of

A

cardiac output and total peripheral resistance (TPR)

91
Q

TPR =

A

the sum of the resistances to flow offered by all the systemic blood vessels

92
Q

MAP =

A

CO x TPR

93
Q

all changes in mean arterial pressure must be the result of changes in

A

cardiac output and/or total peripheral resistance

94
Q

Compensatory changes in arteriolar resistance occur to protect the

A

maintenance of mean arterial pressure

95
Q

Systemic vascular system is a series of tube….therefore delta P =

A

mean systemic artereial pressure (MAP) – pressure in the right atrium.

**BUT: RAP ~O mmHg, so MAP = COXTPR

F = CO and R = TPR

96
Q

MAP is the perfusion pressure for all

A

vascular beds and therefore very important.

97
Q

Baroreceptor neurons function as sensors in the

A

homeostatic maintenance of MAP by constantly monitoring pressure in the aortic arch and carotid sinuses.

98
Q

Baroreceptor neurons deliver MAP information to the

A

medulla oblongata’s cardiovascular control center (CVCC);

the CVCC determines autonomic output to the heart.

99
Q

The information reported by

baroreceptor neurons sets in motion autonomic responses not only to the heart, but also to

A

arterioles and veins.

100
Q

If arterial pressure decreases, the discharge rate of the

A

arterial baroreceptors decreases

101
Q

Fewer impulses travel up the afferent nerves to the medullary cardiovascular center and this induces:

(When arterial baroreceptor discharge rate drops)

A

increased HR because of increased sympathetic activity to the heart and decreased parasympathetic activity

2) increased ventricular contractility because of increased sympathetic activity to the ventricular myocardium
3) arteriolar constriction because of increased sympathetic activity to the arterioles
4) increased venous constriction because of increased sympathetic activity to the veins
- ↑CO (↑ HR ↑ SV) ↑ TPVR  normalization of BP

Sorry about text vomit, know that the reciprocal can occur.

102
Q

an abnormal increase in MAP “squeezes” more fluid out of the blood and into the

A

urine, leading to a reduction in blood volume, which then reduces MAP back closer to the “set point” value.

103
Q

At capillaries, reduced MAP increases

A

absorption and

reduces filtration to help “protect” blood volume.

104
Q

Hypotension - Allergic response

A

Histamine release –> vasodilation

105
Q

Hypotension: Emotional stress

A

↓Sympathetic and ↑Parasympathetic

-vasovagal syncope

106
Q

Pressure at a given point =

A

cardiac generate pressure + pressure equal to the weight of the column of blood to the point measured.

107
Q

Decrease in total peripheral resistance is seen during

A

exercise

108
Q

Increase in CO during exercise

is due to large increase in

A

HR and

smaller increase in SV (stroke volume)

109
Q

VO2max could be limited by:

A

1- cardiac output
2- respiratory system’s ability to deliver oxygen
3- exercising muscle’s ability to use oxygen

110
Q

Except for highly trained athletes –

A

CO is the factor that

determines VO2max

111
Q

Renal hypertension –>

A

increased renin release –>

increased angiotension II release

112
Q

Diastolic dysfunction – reduced

A

ventricular compliance results in an
increase end-diastolic pressure and thus a decreased end-diastolic
volume and a decreased stroke volume.

113
Q

Systolic dysfunction – a decrease in

A

cardiac contractility – a lower

Stroke volume at any given end-diastolic volume.

114
Q

To further increase the stroke volume:

A

fill it more fully with blood
AND
deliver sympathetic signals (norepinephrine and epinephrine);
it will also relax more rapidly, allowing more time to refill

115
Q

Heart failure leads to increased fluid retention, leading to
increased blood volume and greater stroke volume;
however, the failing heart is less able to handle a

A

large EDV.

116
Q

Sudden cardiac death occurs from

A

ventricular fibrillation.

117
Q

Thrombolytic therapy

A

Streptokinase

tissue plasminogen activator

118
Q

Percutaneous coronary intervention

A

Balloon angioplasty

Stenting

119
Q

Stroke volume is regulated through changes in:

A

the END-DIASTOLIC VOLUME (the PRELOAD): the size of the heart just before it contracts
2. cardiac CONTRACTILITY (the amount of free Ca2+ in ventricular muscle cells)

120
Q

The EDV is the volume of the ventricle when it is

A

completely filled, just before it contracts.

sorry, I’m dumb and keep mixing this up

121
Q

larger EDV (PRELOAD) produces a

A

STRONGER contraction and a LARGER SV

Frank sterling mech

122
Q

The length-tension relationship of cardiac muscle is responsible for the

A

Frank-Starling mechanism

123
Q

larger EDV leads to a larger

A

initial fiber length

124
Q

F-s relationship MATCHES the

A

CO to the VENOUS RETURN

125
Q

F-s relationship  it matches the outputs of the

A

two VENTRICLES

126
Q

Sympathetic response increases stroke volume by increasing

A

calcium

Physio Exam 2 (11 decks)

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