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Human physiology > Chapter 14: Cardiovascular Physiology > Flashcards

Chapter 14: Cardiovascular Physiology Flashcards

1
Q
  • the heart
  • blood vessels
  • blood
A

cardiovascular system

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2
Q

what does the cardiovascular system transport?

A
  • oxygen & nutrients to cells
  • wastes from cells
  • hormones, immune cells, and clotting proteins to specific target cells
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3
Q

what is the flow of blood through the cardiovascular system?

A

heart–> arteries–> arterioles—> capillaries –> venules–> veins–> heart

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4
Q

large, branching vessels taking blood away from the heart

A

arteries

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5
Q

small branching vessels with high resistance

A

arterioles

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6
Q

site of exchange between blood and tissue

A

capillaries

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7
Q

small converging vessels

A

venules

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8
Q

relatively large converging vessels that conduct blood to the heart

A

veins

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9
Q

is the cardiovascular system open or closed?

A

closed system

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10
Q

what does the blood consist of?

A
  • erthyrocytes (RBC)
  • leukocytes (WBC)
  • platelets
  • plasma
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11
Q
  • red blood cells

- transport oxygen and carbon dioxide

A

erythrocytes

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12
Q
  • white blood cells

- defend body against pathogens

A

leukocytes

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13
Q
  • cell fragments

- important in blood clotting

A

platelets

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14
Q

fluid and solutes

A

plasma

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15
Q
  • supplied by right heart
  • blood vessels from heart to lungs, and from lungs to heart
  • oxygen diffuses from tissues to blood
A

pulmonary circuit

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16
Q
  • supplied by left heart
  • blood vessels from heart to systemic tissues, and from tissues to heart
  • oxygen diffuses from blood to tissues
A

systemic circuit

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17
Q

how is the flow of blood through systemic and pulmonary circuits?

A

its in series

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18
Q

what is the path of blood in the circuits?

A

Left ventricle → aorta → systemic circuit → vena cavae → right atrium right ventricle → pulmonary artery → pulmonary circuit → pulmonary veins → left atrium → left ventricle

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19
Q
  • located in thoracic cavity

- weighs 250-350 grams

A

heart

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20
Q

separates the abdominal cavity from the thoracic cavity

A

diaphragm

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21
Q
  • Membranous fluid-filled sac surrounding the heart

- Lubricates the heart and decreases friction

A

pericardium

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22
Q

what are the 3 layers of the heart wall?

A
  • epicadium
  • myocardium
  • endothelium
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23
Q

external membrane of heart wall

A

epicardium

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24
Q
  • middle layer of heart wall

- cardiac muscle

A

myocardium

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25
Q
  • inner layer of heart wall

- layer of endothelial cells

A

endothelium

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26
Q

drives blood flow

A

pressure difference (high pressure to low pressure)

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27
Q

what is the normal direction of blood flow?

A
  • atria to ventricles

- ventricles to arteries

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28
Q
  • prevent backward flow of blood

- open passively based on pressure gradient

A

valves

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29
Q

what are the two main valves of the heart?

A
  • Atrioventricular (AV) valves

- semilunar valves

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30
Q

tricuspid valve

A

Right AV valve

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31
Q

bicuspid valve = mitral valve

A

Left AV valve

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32
Q

Keep AV valves from being pushed back into atrium

A

Papillary muscles and chordae tendineae

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33
Q
  • aortic valve

- pulmonary valve

A

semilunar valves

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34
Q

what happens when the ventricles are relaxed?

AV valves

A

blood enters the atria, pushing the atrioventricular valve cusps down into the ventricles, opening the valves

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35
Q

what happens when the ventricles contract?

AV valves

A

blood presses up against the atrioventricular valve cusps, forcing the valves closed

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36
Q

what happens when papillary muscles contract?

A

tightens the chordae tendineae, preventing the

valve cusps from being pushed into the atria

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37
Q

are the AV valves open or closed during ventricular contraction?

A

AV valves remain closed
to prevent blood flow
backward into the atria.

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38
Q

what happens when the ventricles contract?

semilunar valves

A

blood presses up against the semilunar valve cusps, forcing the valves open and allowing blood to flow into the aorta and pulmonary
artery

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39
Q

what happens when the ventricles relax?

semilunar valves

A

blood in the aorta and pulmonary artery presses down against the valve cusps, forcing them to close

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40
Q

prevent blood that has entered the arteries from flowing back into the ventricles during
ventricular relaxation.

A

semilunar valves

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41
Q

ensured by the two sets of valves

A

one-way flow of blood through the heart

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42
Q

drive blood flow from high pressure to low pressure

A

pressure gradients

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43
Q

flow due to pressure gradients

A

bulk flow

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44
Q

creates a pressure gradient for bulk flow of blood

A

the heart

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45
Q

what must exist in the circulatory system to maintain blood flow?

A

a gradient

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46
Q

the force exerted by blood

A

pressure

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47
Q

in which direction does blood flow occur?

A

from high pressure to low pressure

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48
Q

the force pushing blood against the various factors resisting the flow of liquid in a pipe

A

ΔP

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49
Q

what is flow proportional to?

A

ΔP

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50
Q
  • the pressure exerted on the walls of the container by the fluid within the container
  • proportional to the height of the water column
A

hydrostatic pressure

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51
Q
  • depends on the pressure gradient

- only if there is a positive pressure gradient (ΔP)

A

fluid flow through a tube

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52
Q

depends on the pressure gradient (ΔP), not the absolute pressure (P)

A

blood/fluid flow

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53
Q

is the pressure gradient greater in the systemic circuit or the pulmonary circuit?

A

it is much greater in the systemic circuit

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54
Q

is the flow greater in the systemic or pulmonary circuit?

A

flow is equal in both circuits

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55
Q

=ΔP/R

A

flow

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56
Q

is resistance less in the pulmonary or systemic circuit?

A

resistance through the pulmonary circuit is much less than resistance through the systemic circuit

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57
Q

inversely proportional to resistance

A

flow through a tube

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58
Q

what happens if resistance increases?

A

flow decreases

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59
Q

what happens if resistance decreases?

A

flow increases

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60
Q
  • Resistance is proportional to length (L) of the tube (blood vessel)
  • Resistance is proportional to viscosity (), or thickness, of the fluid (blood)
  • Resistance is inversely proportional to tube radius to the (coffee straw)
A

Poiseuille’s Law

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61
Q

proportional to length (L) of the tube (blood vessel)

A

resistance
-Resistance increases as
length increases (long
straw)

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62
Q

proportional to viscosity (), or thickness, of the fluid (blood)

A

resistance
-Resistance increases as
viscosity increases
(milkshake)

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63
Q

inversely proportional to tube radius to the (coffee straw)

A

resistance
-Resistance decreases
as radius increases

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64
Q

has a large effect on resistance to blood flow (flow rate)

A

small change in radius of blood vessel

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65
Q
  • decrease in blood vessel diameter/radius

- decreases blood flow

A

vasoconstriction

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66
Q
  • increase in blood vessel diameter/radius

- increases blood flow

A

vasodilation

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67
Q

the volume of blood that passes a given point in the system per unit time (how much)

A

flow rate

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68
Q

the distance a fixed volume of blood travels in a given period of time (how fast)

A

velocity of flow

69
Q

when is velocity directly related to flow rate?

A

when the tube has a fixed diameter

70
Q

when does the velocity varies inversely with diameter?

A

when the tube has a variable diameter

71
Q

faster in narrow sections

A

velocity of blood flow

72
Q

slower in wider sections

A

velocity of blood flow

73
Q

what does cardiac muscle consist of ?

A
  • contractile cells

- autorhythmic cells (pacemakers)

74
Q

Striated fibers organized into sarcomeres

A

contractile cells

75
Q
  • Signal for contraction

- Do not have organized sarcomeres

A

Autorhythmic cells, or pacemakers

76
Q

branched, have a single nucleus, and are attached to each other by specialized junctions known as intercalated disks.

A

myocardial muscle

77
Q

contain desmosomes

that transfer force from cell to cell, and gap junctions that allow electrical signals to pass rapidly from cell to cell

A

intercalated discs

78
Q
  • Spontaneously depolarizing membrane potentials generate action potentials
  • Coordinate and provide rhythm to heartbeat
A

pacemaker cells

79
Q
  • Rapidly conduct action potentials initiated by pacemaker cells to myocardium
  • Conduction velocity = 4 meters/second
A

conduction fibers

80
Q
  • Sinoatrial node
    * Pacemaker of the heart
  • Atrioventricular node
A

pacemaker cells of the myocardium

81
Q

what are the conduction fibers of the myocardium?

A
  • Internodal pathways
  • Bundle of His
  • Purkinje fibers
82
Q
  • Sets the pace of the heartbeat at 70 bpm

- AV node (50 bpm) and Purkinje fibers (25–40 bpm)

A

sinoatrial (SA) node

83
Q

Routes the direction of electrical signals so the heart contracts from apex to base

A

Internodal pathway from SA to atrioventricular (AV) node

84
Q
  • SA node → right atrium → left atrium
  • rapid
  • Simultaneous contraction of right and left atria
A

interatrial pathway

85
Q

-SA node → AV node

A

internodal pathway

86
Q
  • Only pathway from atria to ventricles
  • Slow conduction: AV nodal delay = 0.1 sec
  • Atria contract before ventricles
A

AV node transmission

87
Q

how does ventricular excitation occur?

A
  • Down bundle of His
  • Up Purkinje fibers
  • Purkinje fibers contact ventricle contractile cells
  • Ventricle contracts from apex up
88
Q

what is the conduction system of the heart?

A

SA node–>internodal pathways–> AV node–>AV bundle–> bundle branchea–>purkinje fibers

89
Q

how do pacemakers control the heartbeat?

A
  • autorhythmic cells
  • spontaneous depolarization
  • depolarize to threshold
  • repolarization
90
Q

have pacemaker potentials

A

autorhythmic cells

91
Q

**caused by closing K+ channels and opening two types of channels
-Na+ funny channels (If):
net depolarization
-Ca2+ channels (T-type):
further depolarization

A

spontaneous depolarizations

92
Q

how is the heart depolarized to threshold?

A

Open fast Ca2+ channels(L-type): action potential

93
Q

how is the heart repolarized?

A

open K+ channels

94
Q

gradually becomes less negative until it reaches threshold, triggering an action potential

A

pacemaker potential

95
Q
  • Depolarization due to Na+ entry
  • Repolarization due to K+ exit
  • Long action potential (plateau) due to Ca2+ entry in the cell prevents tetanus
A

myocardial contractile cells

96
Q

lasts almost as long as the entire muscle twitch

A

refractory period in cardiac muscle fiber

97
Q

prevents tetanus

A

long refraction period in cardiac muscle

98
Q

refractory period is very short compared with the amount of time required for the development of tension

A

skeletal muscle fast-twitch fiber

99
Q

if they are stimulated repeatedly, it will exhibit summation and tetanus

A

skeletal muscles

100
Q

how does cardiac muscle compare to skeletal muscle?

A
  • smaller & have single nucleus per fiber
  • branch & join neighboring cells through intercalated disks (desmosomes & gap junctions)
  • T-tubules are larger & branch
  • sarcoplasmic reticulum is smaller
  • mitochondria occupy 1/3 of cell volume
101
Q

allow force to be transferred

A

desmosomes

102
Q

provide electrical connection

A

gap junctions

103
Q

how is excitation-contraction coupling in cardiac muscle similar to properties of skeletal muscle?

A
  • T-tubules
  • Sarcoplasmic reticulum Ca2+
  • Troponin-tropomyosin regulation
104
Q

how is excitation-contraction coupling in cardiac muscle similar to properties of smooth muscle?

A
  • gap junctions

- Extracellular Ca2+

105
Q

what are the steps of excitation-contraction coupling of the heart?

A
  1. Depolarization of cardiac contractile cell to threshold via gap junction
  2. Opening of calcium channels in plasma membrane
  3. AP travels down T tubules
  4. Calcium is released from sarcoplasmic reticulum
  5. Calcium binds to troponin, causing a shift in tropomyosin
  6. Binding sites for myosin on actin are exposed
  7. Crossbridge cycle occurs
106
Q

how is calcium released from sarcoplasmic reticulum?

A
  • calcium-induced calcium release

- action potentials in T tubules

107
Q
  • Provides information on heart rate and rhythm, conduction velocity, and even the condition of tissues in the heart.
  • has waves and sements
A

electrocardiogram

108
Q

what are the components of an electrocardiogram?

A
  • P wave
  • QRS complex
  • T wave
  • PR segmet
109
Q

shows atrial depolarization

A

P wave

110
Q

shows ventricular depolarization and atrial repolarization

A

QRS complex

111
Q

shows ventricular repolarization

A

T wave

112
Q
  • shows AV nodal delay

- conduction through AV nodes and AV bundle

A

PR segment

113
Q

what does an upward deflection on an ECG mean?

A

means the current flow vector is toward the positive electrode

114
Q

what does a downward deflection on an ECG mean?

A

the current flow vector is toward the negative electrode

115
Q

what does no deflection on an ECG mean?

A

the vector is perpendicular to the axis of the electrode

116
Q
  • lag behind electrical events

- contraction follows action potential

A

mechanical events

117
Q

begins with atrial depolarization, atrial contraction at the end of P wave

A

ECG

118
Q

goes through AV node and AV bundle

A

PR segment signal

119
Q

ventricular contraction begins and continues through T wave

A

Q wave end

120
Q
  • loss of conduction through the AV node
  • P wave becomes independent of QRS
  • atrial and ventricular contractions are independent
A

third degree heart block

121
Q
  • loss of coordination of electrical activity of the heart

- death can ensue within minutes unless corrected

A

ventricular fibrillation

122
Q

-Events associated with the flow of blood through the heart during a single complete heartbeat

A

cardiac cycle

123
Q

what are the two main periods of the cardiac cycle?

A
  • systole: ventricle contraction

- diastole: ventricle relaxation

124
Q

open passively due to pressure gradients

A

valves

125
Q

open when atrial pressure > ventricular pressure

A

AV valves

126
Q

open when ventricular pressure > arterial pressure

A

semilunar valves

127
Q

what are the phases of the cardiac cycle?

A
  1. Ventricular filling
  2. isovolumetric ventricular contraction
  3. ventricular ejection
  4. Isovolumetric ventricular relaxation
128
Q
  • Middle of ventricular diastole
  • Venous return
  • AV valve opens
  • Blood moves from atria to ventricle
  • Pulmonary and aortic valves are closed
  • Passive until atrium contracts
A

ventricular filling

129
Q
  • start of systole
  • ventricle contracts-increases pressure
  • AV & semilunar valves closed
  • no blood entering or exiting the ventricles
A

Isovolumetric ventricular contraction

130
Q
  • Remainder of systole
  • Pressure in ventricles > pressure in arteries
  • Semilunar valves open
  • Ventricular pressure < aortic pressure
  • Semilunar valves close
A

ventricular ejection

131
Q
  • Onset of diastole
  • Ventricle relaxes—decreases pressure
  • AV and semilunar valves closed
  • No blood entering or exiting ventricle
A

Isovolumetric ventricular relaxation

132
Q
  • Atrial pressure rises slowly with filling of blood
  • Ventricular pressure is low
  • Small rise in VP at end due to atrial contraction
A

Phase 1

133
Q
  • Rapid rise in ventricular pressure

- Atrial pressure falls

A

Phase 2

134
Q
  • Ventricular pressure falls

- Atrial pressure falls further until late systole

A

Phase 3

135
Q
  • Aortic valve closes
  • Blood is still leaving aorta, so pressure falls
  • Lowest point = diastolic pressure
A

Diastole

136
Q
  • Aortic valve opens
  • Pressure rises rapidly with ejection
  • Highest point = systolic pressure
  • Aortic valve closes
  • Backflow of blood causes slight increase—dicrotic notch
A

systole

137
Q
  • maintains blood flow through the entire cardiac cycle

- continuous blood flow during cardiac cycle

A

aortic pressure

138
Q
  • elastic
  • pressure reservoir
  • stores energy during systole as walls expand
  • releases energy during diastole as walls recoil inward
A

aorta (and large arteries)

139
Q

Volume of blood in ventricle at the end of diastole

A

EDV: end-diastolic volume

140
Q

Volume of blood in ventricle at the end of systole

A

ESV: end-systolic volume

141
Q

-Volume of blood ejected from ventricle each cycle

=EDV-ESV
=130 mL-60 mL = 70 mL

A

SV: stroke volume

142
Q

-fraction of end-diastolic volume ejected during a heartbeat

=stroke volume/end diastolic volume
=70 mL/130 mL = 0.54 (i.e. 54% at rest)

A

ejection fraction (EF)

143
Q

-Volume of blood pumped by each ventricle per minute

=SV x HR

A

cardiac ouotput

144
Q
  • average= 5liters/min at rest

- 72 beats min x 0.07 L/beat = 5.0 L/min

A

cardiac output

145
Q

average blood volume of cardiac output

A

5.5 liters

146
Q

determined by SA node firing frequency

A

heart rate

147
Q

SA node intrinsic firing rate

A

100/min

148
Q

is there extrinsic control on the heart from the SA node?

A

no, HR=100

149
Q

under control of ANS and hormones

A

SA node

150
Q
  • at rest

- HR=75

A

parasympathetic system dominates

151
Q
  • excitement

- HR increases

A

sympathetic system takes over

152
Q

what does the Activity of sympathetic neurons projecting to SA node do to the HR?

A

raises HR

153
Q

what does the Activity of parasympathetic neurons projecting to SA node do to the HR?

A

lowers HR

154
Q

what do levels of circulating epinephrine do to the HR?

A

raises HR

155
Q

what does stimulation by the parasympathetic nerves do to the heart rate?

A

decreases heart rate

156
Q

what does stimulation by sympathetic nerves do to the heart rate?

A

increases heart rate

157
Q

how does increased sympathetic activity come about?

A

nerves or epinephrine–> beta 1 receptors in SA node –> increase open state of I_f and Ca2+ channels–> increase rate of spontaneous depolarization–> increase heart rate

158
Q

depolarize the autorythmic cell and speed up the pacemaker potential, increasing the heart

A

sympathetic stimulation

159
Q

what does increased parasympathetic activity do?

A

vagus nerve–>muscarinic cholinergic receptors in SA node–>increase open state of K+ channels & closed sate of Ca2+ channels—> decrease rate of spontaneous depolarization & hyperpolarize cell —> decrease heart rate

160
Q

hyperpolarizes the membrane potential of the autorhythmic cell & slows depolarization, slowing down the heart rate

A

parasympathetic stimulation

161
Q

what are the primary factors affecting stroke volume?

A
  • ventricular contractility
  • end-diastolic volume
  • afterload
162
Q

how does ventricular contractility affect stroke volume?

A

-a more forceful contraction will expel more blood

163
Q

what is involved in the sympathetic control of ventricular contraction?

A
  • sympathetic innervation of muscle cells

- Norepinephrine → β1 adrenergic receptors → cAMP second-messenger system

164
Q

what are the steps involved in norepinephrine leading to the CAMP second messenger system?

A
  1. Augment open Ca2+ channels
  2. Increase Ca2+ release from sarcoplasmic reticulum (SR)
  3. Increase myosin ATPase rate
  4. Enhance rate of Ca2+ -ATPase activity on SR
165
Q

what is the influence of end-diastolic volume on stroke volume?

A

***starlings law
-Increased EDV
stretches muscle fibers
-Fibers closer to optimal
length
-Optimal length →
greater strength of
contraction
-Result → increased SV—
–> increase venous
return—–> increase
strength of contraction–
–> increase stroke
volume

166
Q

what does an increase in EDV cause?

A

stroke volume to increase

167
Q

what are the factors affecting end-diastolic volume?

A
  • end diastolic pressure
    • filling time
    • atrial pressure
    • central venous pressure
  • afterload
168
Q

preload

A

end-diastolic pressure

169
Q

pressure in aorta during ejection

A

afterload

Human physiology (17 decks)

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