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Anatomy 403 > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

the heart

A
  • size of fist
  • between ribs 2-5
  • 2/3 length at midline
  • weighs 10 oz.
  • beats 3 billion times in lifetime (80 years)
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2
Q

anatomical axis of heart

A

45 degrees

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3
Q

what are the four chambers of the heart?

A
  • right atrium
  • left atrium
  • right ventricle
  • left ventricle
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4
Q

what are the four valves of the heart?

A
  • 2 AV valves

- 2 semilunar valves

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5
Q

papillary muscles

A

attach to tendinous cords

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6
Q

tendinous cords

A

attack to cusps of AV valves to keep them from prolapsing into atria

  • don’t pull valves open
  • act only to limit movement
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7
Q

cardiac muscle

A

myocardium

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8
Q

what are the semilunar valves?

A
  • aortic valve

- pulmonary valve

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9
Q

what are the AV valves?

A
  • bicuspid valve

- tricuspid valve

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10
Q

semilunar valves

A

3 cusps with “pockets”

- when blood flows back, closes valve

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11
Q

stenosis

A

narrowed opening due to scar tissue

  • when blood is flowing through
  • makes whistle sound
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12
Q

stenosis causes

A
  • increased BP causing increased wear / tear

- rheumatic fever = antibodies attack valves

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13
Q

valvular insufficiency

A

valves don’t close properly blood leaks backward (regurgitation)
- makes a gurgling sound

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14
Q

what is the mot commonly replaced valve?

A

mitral value

bicuspid valve

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15
Q

pulmonary

A
  • right side
  • low pressure
  • about 10 mm Hg
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16
Q

systemic

A
  • left side
  • high pressure
  • about 110 mm Hg
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17
Q

blood flow through the heart

A
  1. superior and inferior vena cava
  2. right atrium
  3. tricuspid value
  4. right ventricle
  5. pulmonary valve
  6. pulmonary trunk
  7. R/L pulmonary artery
  8. lungs
  9. pulmonary veins
  10. left atrium
  11. bicuspid valve
  12. left ventricle
  13. aortic valve
  14. aorta
  15. systemic capillaries
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18
Q

cardiac muscle tissue

A
  • short, branched cells connected by intercalated discs
  • involuntary
  • aerobic respiration only
  • –> lots of mitochondria (no fatigue)
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19
Q

syncytium

A

intercalated discs contain gap junctions so that cells contract in unison

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20
Q

all three muscle types are similar by:

A
  • sliding filaments
  • ATP power
  • elevated Ca+2 triggers
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21
Q

cardiac muscle is like skeletal by:

A
  • sarcomeres
  • striations
  • troponin
  • t-tubules
  • SR Ca+2
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22
Q

cardiac muscle is like smooth by:

A
  • small, single nucleus
  • pacemaker cells
  • gap junctions (syncytium)
  • autonomic/hormones modulate
  • Ca+2 entry from outside
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23
Q

EC coupling in cardiac muscle

A
  • Ca+2 flow thru the DHPR (L-type Ca+2 channel) opens the RyR releasing Ca+2 from the SR. The Ca+2 induces additions Ryr channels to open
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24
Q

CIRI

A

Ca+2 induced Ca+2 release

- positive feedback

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25
Q

autorhythmic cells (pacemaker cells)

A
  • <1% of cells
  • determine HR
  • myogenic
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26
Q

myogenic

A
  • can contract without nervous system input
  • beat on its own
  • ex: SA node (75 bpm) , AV node (45 bpm)
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27
Q

conducting cells

A

spread electrical stimulus

  • ex: bundle of his (AV bundle) , bundle branches, purkinje fibers
  • all of these also have pacemaker activity
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28
Q

contractile cells

A
  • 99%
  • myocardium
  • all have gap junctions –> AP spreads from one cell to another
  • every heart cell contracts with every beat
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29
Q

electrical conduction system

A
  1. SA node fires
  2. excitation spreads through myocardium
    - atrial contraction (systole)
  3. AV node fires
  4. excitation spreads down AV bundle
  5. purkinje fivers distribute excitation through ventricular myocardium
    - ventricular contraction
    - 3-5 are fast
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30
Q

electrical conduction through myocardium

A
  1. atria contract in unison
  2. delay at AV node (ventricles fill)
  3. ventricles contract in unison
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31
Q

sinus rhythm

A

normal heartbeat triggered by the SA node

- about 75 bpm

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32
Q

ectopic focus

A

any region of spontaneous firing other than SA node

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33
Q

nodal rhythm

A
  • AV node produces this
  • backup pacemaker
  • about 45 bmp
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34
Q

bundle of his/bundle branches/purkinje fibers

A
  • < 35 bpm

- not fast enough to sustain life

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35
Q

pacemaker potentials of nodal cells

A
  • Na+ enters = Na+ leak channels always open = no stable RMP
  • Ca+2 enters (depolarization) = VG Ca+2 channels
  • myogenic (beats on its own)
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36
Q

action potential in contractile cells

A
  1. only depolarize when stimulated (no potential activity) VG Na+ channel
  2. Na+2 inflow depolarizes membrane and triggers opening of more Na+ channels (positive feedback) and rapid increase in voltage change
  3. Na+ channels close and voltage peaks at +30 mV
  4. Ca+2 and K+ channels open and inflow of Ca+2 prolongs repolarization (K+ out)
  5. Ca+2 channels close and K+ outflow returns membrane to RMP
    - 99% of myocardium
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37
Q

cardiac muscle AP

A
  • have long refractory period to prevent tetanus

- no temporal summation

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38
Q

electrocardiogram (EKG)

A
  • composite recording of all electrical activity in heart
  • not directly APs
  • used to determine heath of heart
  • HR, regularity, size, position of chambers, damage
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39
Q

Einthoven’s Triangle

A

combination of 12 leads uses a different combination of reference and recording electrodes to provide different angles for “viewing” the heart

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40
Q

standard limb leads

A
  • lead I
  • lead II
  • lead III
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41
Q

augmented limb leads

A
  • aVR
  • aVL
  • aVF
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42
Q

pericardial (chest) leads

A

use limb leads combined into a reference point at the center of the heart
- V1 - V6

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43
Q

P wave

A

atrial depolarization

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44
Q

PQ segment

A
  • atrial contraction

- delay at AV node

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45
Q

QRS complex

A
  • ventricular depolarization

- atrial repolarization

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46
Q

ST segment

A

ventricular contraction

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47
Q

T wave

A

ventricular repolarization

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48
Q

TP interval

A

diastole

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49
Q

average MEA

A

59˚

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50
Q

normal range MEA

A

-30˚ - +110˚

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51
Q

MEA

A

tells us the net direction depolarization is heading

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52
Q

QRS complex is highly positive

A

electrical axis is parallel to that lead

- normal

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53
Q

QRS complex is highly negative

A

electrical axis is in opposite direction to that lead (inverted QRS)

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54
Q

QRS complex is isoelectric

A

perpendicular to that lead

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55
Q

left axis deviation (LAD)

A

MEA < -30˚

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56
Q

causes of left axis deviation

A
  1. left ventricular hypertrophy
  2. right ventricular destruction
  3. altered body structure
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57
Q

left ventricular hypertrophy:

A
  • from increased BP

- mitral / aortic valve stenosis

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58
Q

right ventricular destruction:

A

from heart attack (myocardial infarction –> MI)

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59
Q

altered body structure from LAD

A

short, obese

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60
Q

pathologic hypertrophy

A

either ventricle, the axis will shift in direction of hypertrophied ventricle

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61
Q

right axis deviation (RAD)

A

MEA > 110˚

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62
Q

causes of right axis deviation

A
  1. right ventricular hypertrophy
  2. left ventricular destruction
  3. altered body stature
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63
Q

right ventricular hypertrophy

A
  • caused by pulmonary hypertension

- tricuspid / pulmonary stenosis

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64
Q

left ventricular destruction

A

heart attack (MI)

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65
Q

altered body structure from RAD

A

extremely tall, thin

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66
Q

bradycardia

A

HR < 60 bpm

- increased TP interval

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67
Q

tachycardia

A

HR > 100 bpm

- decreased TP interval

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68
Q

artificial pacemaker

A

surgically implanted to provide electrical stimulus (artificial depolarization) to take over for either SA node or AV node

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69
Q

types of artificial pacemakers

A
  1. constant pacemaker

2. demand pacemaker

70
Q

constant pacemaker

A

constantly fire and set HR

71
Q

demand pacemaker

A

fires when needed

72
Q

when do you need a pacemaker

A
  • possibly if SA node fails
    • any exertion requiring increased HR would be difficult to sustain
  • ALWAYS if AV node fails = only electrical link to ventricles
73
Q

function of heart

A

to create pressure gradient

74
Q

how does pressure flow?

A

high pressure to low pressure

75
Q

pressure of atria

76
Q

pressure of arteries

77
Q

pressure of ventricles

78
Q

AV valves open

A

P atria > P ventricles

79
Q

AV valves closed

A

P ventricles > P atria

80
Q

SL valves open

A

P ventricles > P arteries

81
Q

SL valves closed

A

P arteries > P ventricles

82
Q

phase 1 of cardiac cycle

A
  • TP interval
  • ventricular filling –> blood flows into ventricles
  • atria relaxed
  • ventricles relaxed
  • P wave –> PQ segment
  • atria contract
  • ventricles relaxed
  • AV valves: open
  • aortic and pulmonary valves: closed
  • P atria > P ventricles
  • EDV
83
Q

End diastolic volume (EDV)

A

about 130 mL

84
Q

phase 2 of cardiac cycle

A
  • isovolumetric ventricular contraction
  • QRS complex –> beginning of ST segment
  • atria relaxed
  • ventricles contract
  • AV valves: closed
  • —> close first
  • aortic and pulmonary valves: closed
  • P ventricles > P atria
  • P ventricles < P arteries
85
Q

isovolumetric ventricular contraction

A
  • same volume –> tension but no blood flow
  • volume stays same because all valves closed
  • as P ventricles increase, AV valves closes P ventricles > P atria
86
Q

phase 3 of cardiac cycle

A
  • ventricular ejection = blood flows out of ventricle
  • ST segment
  • atria relaxed
  • ventricles contract
  • AV valves: closed
  • aortic and pulmonary valves: open
  • P ventricles > P arteries
  • stroke volume
87
Q

stroke volume average

A

about 70 mL

88
Q

phase 4 cardiac cycle

A
  • isovolumetric ventricular relaxation
  • T wave
  • atria relaxed
  • ventricles relaxed
  • AV valves: closed
  • aortic and pulmonary valves: closed
  • P ventricules < P arteries
  • end systolic volume
89
Q

end systolic volume

A

about 60 mL

90
Q

isovolumetric ventricular relaxation

A
  • as P ventricle decreases, SL valves close

- volume stays because all valves closed

91
Q

end systolic volume

A

about 60 mL

92
Q

AV valves close

93
Q

SL valves close

94
Q

pressure-volume loop: one cardiac cycle

A

left ventricular pressure (LVP) is plowed against left ventricular volume (LVV) at multiple time points during a complete cardiac cycle

95
Q

ESV equation

A

EDV - SV = ESV

96
Q

pulmonary edema

A
  1. right ventricular output exceeds left ventricular
  2. pressure backs up
  3. fluid accumulates in pulmonary tissue
  • left ventricular failure
97
Q

systemic edema

A
  1. left ventricular output exceeds right ventricular output
  2. pressure backs up
  3. fluid accumulates in systemic tissue
  • right ventricular failure
  • -> feet/ankles
  • -> abdominal cavity (ascites)
98
Q

cardiac output

A

volume of blood pumped by each ventricle per minute

99
Q

equation for cardiac output

A

CO = HR x SV

100
Q

regulation of HR

A

chronotropic agents

101
Q

positive chronotropic agents

A

increase HR:

  • SNS (NE)
  • Epi
  • caffeine, nicotine
102
Q

negative chronotropic agents

A

decrease HR:

  • PSNS (Ach)
  • PSNS affects only HR not SB
103
Q

average CO

A

5.25 L/min

104
Q

sympathetic

A

cardio accelerator center (medulla)

105
Q

parasympathetic

A

cardio inhibitory venter (medulla)

106
Q

sympathetic atria

A

increase HR

107
Q

sympathetic ventricles

A

increases SV

108
Q

vagal tone

A

holds resting HR lower

109
Q

effect of SNS on HR

A

increase pacemaker potential (NE opens more Na+ channels)

110
Q

effects of PSNS of HR

A

decrease pacemaker potential (Ach opens K+ channels)

111
Q

stroke volume

A

volume of blood ejected by each ventricle per beat

112
Q

regulation of stroke volume

A
  1. preload
  2. contractility
  3. afterload
113
Q

preload

A

tension (stretch) in ventricles before contracting = EDV
- increased EDV = increased SV

  • increased venous return = increased EDV = increased stretch = increase force of contraction = increased SV
114
Q

contractility

A

how hard the myocardium contracts for a given preload

  • inotropic agents
  • increased contractility = increased SV
115
Q

positive inotropic agents

A

factors that increase Ca+2:

  • SNS, NE, Epi
  • glucagon (increases cAMP)
  • digitalis (increases Ca+2 in cytoplasm)
116
Q

digitalis

A

used to treat CHF

117
Q

negative inotropic agents

A
  • increased K+ (decreased AP strength) = decreased Ca+2 release
  • NOT PSNS –> no input to ventricles
118
Q

afterload

A

forces ventricles must overcome to pump blood = BP in arteries

  • increased BP = decreased SV
  • don’t want this high
119
Q

ESPVR

A

end diastolic pressure volume relationship

- represents max pressure that is developed by left ventricle

120
Q

pressure - volume loop: exercise

A
  1. increase HR = increase HR + increase SV = increase CO = increased BP = increased A2
  2. increased SNS = increased contractility (increased Epi) = increased C2 = increased SV2
  3. increased skeletal contraction = increased venous return = increased EDV = increased P2 = increased SV2
121
Q

pressure - volume loop: heart failure

A
  • decreased contractility (decreased Ca+2) = increased ESV2 (decreased SV2) –> decreased BP (decreased A2)
122
Q

compensate for heart failure

A

increased EDV and increased P2, but isn’t enough for increased ESV so there is a decreased CO

123
Q

pressure - volume loop: hypertension

A

increased A2 = decreased SV
to compensate increased SNS = increased HR to maintain CO
–> increased C2
–> P1 doesn’t change

124
Q

arteries

A

away from heart

125
Q

∆P

A

difference in pressure NOT absolute pressure

- increased F = increased ∆P

126
Q

where should you measure blood pressure?

A

on brachial artery with a sphygmomanometer

127
Q

blood pressure

A

systolic pressure / diastolic pressure

128
Q

average blood pressure

A

120 mmHg / 75 mmHg

129
Q

pulse pressure (PP)

A

measure of stress exerted on small arteries by pressure surges generated by the heart

130
Q

pulse pressure equation

A

PP = systolic - diastolic

131
Q

pulse pressure average

132
Q

mean arterial pressure (MAP or MABP)

A
  • another measure of stress on blood vessels

- has most influence on risk of vessels disorders

133
Q

mean arterial pressure equation

A

MAP = diastolic + PP / 3

134
Q

mean arterial pressure average

135
Q

hypotension

A

chronic decrease in blood pressure <90/60 mmHg

136
Q

hypertension

A

chronic increase in blood pressure >140/90 mmHg

137
Q

during systolic flow, if the artery is not elastic

A
  • allow for very fast flow

- BP = 380 mmHg

138
Q

during diastolic flow, if the artery is not elastic

A
  • no flow

- BP = 0 mmHg

139
Q

importance of arterial elasticity

A

elastic recoil exerts pressure on arteries to keep blood moving during diastole

  • decrease pressure fluctuations
  • decreased stress on heart and vessels
140
Q

arteriosclerosis

A

loss of elasticity

- increase BP with age

141
Q

where is the lowest pressure found?

A

venae cavae

142
Q

vasodilation

A

increased radius = decreased resistance = increased flow

- decreased TPR

143
Q

vasoconstriction

A

decreased radius = increased resistance = decreased flow

- increased TPR

144
Q

resistance in vessels

A

TPR Total peripheral resistance

145
Q

increased SNS on vasomotor tone

A

increased SNS = increased vasoconstriction = increased TPR

146
Q

decreased SNS on vasomotor tone

A

decreased SNS = increased vasodilation = decreased TPR

147
Q

vasomotor tone

A

blood vessels are always somewhat constricted

148
Q

two purposes of vasomotion

A
  1. redirect blood flow
  2. ∆ TPR for ∆ BP
    - -> increased TPR = increased BP
    - -> decreased TPR = decreased BP
149
Q

exercise: blood flow

A
  • brain always gets the same
  • increase: muscles, skin, heart
  • decrease: kidneys, digestive
150
Q

veins

A
  • low resistance, high compliance
  • “capacitance vessels”
  • toward the heart
151
Q

venous return is helped by

A
  1. SNS –> vasoconstriction of veins
  2. skeletal muscle ‘pump’
  3. respiratory ‘pump;
152
Q

exercise enhances these mechanisms

A
  • increased SNS activity

- increased venous return = increased EDV (P1) = increased SV = increased CO

153
Q

valve closed during venous return

A

valve prevents backlog between muscle contractions

154
Q

arrangement of vascular beds

A
  • each tissue gets same quality of blood and can regulate what tissues get blood
  • in parallel
155
Q

local control (augoregulation)

A

ability of tissue to regulate own blood supply

- increase wastes (increase CO2, increase H+) and decrease O2 = vasodilation

156
Q

neural (rapid / short term) BP control

A

baroreceptors in carotid sinus and aortic arch = stretch receptors

  • send info to cardiac and vasomotor centers in medulla oblongata
  • always have tone:
    • increase stretch (increase BP) = increase firing rate
    • decrease stretch (decrease BP) = decrease firing rate
157
Q

hormonal (long term) BP control

A

via changes in blood pressure and blood volume

158
Q

what is the main form from the renin-angiotensin-aldosterone system

A

angiotensin II

159
Q

main effects of angiotensin II

A
  1. activates thirst center at hypothalamus, increase ADH
  2. widespread vasoconstriction
  3. adrenal cortex secrete aldosterone
160
Q

angiotensin II

A

vasoconstriction (increase TPR), increase ADH, increase aldosterone
- increase BP

161
Q

aldosterone

A

increase Na+ reabsorption in kidney, water follows Na+ (isotonic)
- increase BV = increase BP

162
Q

antidiuretic hormone (ADH)

A

increase water reabsorption in kidney

- increase BV = increase BP

163
Q

atrial natriuretic peptide (ANP)

A

released from right atrium in response to increased stretch

  • decreased aldosterone
  • decreased ADH
  • decreased Na+ reabsorption in kidney (decreased water)
  • vasodilation
  • decreased BP
164
Q

primary hypertension

A
  • most common
  • unknown cause
  • genetic and environmental factors play role
  • -> obesity, diet, lack of exercise, smoking
165
Q

secondary hypertension

A
  • kidney damage (increase RAA)

- endocrine disorder (increase cortisol, increase aldosterone, increase TH)

166
Q

consequences of hypertension

A
  • heart failure –> from hypertrophy = pumping against increased pressure
  • atherosclerosis / vascular disease –> MI, stroke, kidney failure
167
Q

treatments of hypertension

A

goal = decrease cardiac output and/or decrease TPR

  • decreased CO
  • –> diuretics to decrease BV
  • –> beta blockers to decrease HR
  • decreased TPR
  • –> ACE inhibitors decrease TPR
168
Q

atherosclerosis

A

artery walls thicken with plaques made of WBC’s, cholesterol, and connective tissue
- damage to endothelium = increased inflammation = platelets, WBCs, LDL cholesterol accumulates

169
Q

atherosclerosis consequences

A

vascular disease

    • coronary artery disease
    • peripheral artery disease
    • stroke / TIA
170
Q

embolism

A

blood clot (in veins) or plaque fragment traveling through blood stream

Anatomy 403 (13 decks)

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