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A&P lecture 2 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What type of loop is the CVS

A

Closed loop

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2
Q

Functions of the CVS

A

Transport of materials
Communication between cells

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3
Q

What does the CVS transport

A

Nutrients (Macros)
Wastes (CO2)
Water
Gases (O2)
Heat (sweat, shivering)

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4
Q

How does CVS contribute to communication of cells

A

Hormones, Cytokines, immune system functions

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5
Q

Cytokines

A

Chemicals released by any immune cells, NOT antibodies
Ex: Histamine

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6
Q

Components of CVS

A

Heart, Blood, Blood vessels

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7
Q

Blood vesseles

A

Arteries, arterioles, capillaries, veins, venules

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8
Q

2 loops of the CVS

A

Systemic circulation
Pulmonary circulation

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9
Q

Systemic circulation

A

Blood flows from heart to tissues back to heart
Left heart

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10
Q

Pulmonary circulation

A

Blood flows from heart to lungs back to heart
Right heart

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11
Q

Difference between arteries and veins

A

An artery carries blood away from the heart
Vein carries blood TO the heart

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12
Q

What is special about renal and digestive circulation

A

They have 2 capillary beds instead of 1 (Portal system)

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13
Q

Pressure Gradient

A

A difference in pressure
It dictates how blood move through the body. Moves from high to low pressure

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14
Q

What happens to pressure as blood travels away from heart

A

The mean blood pressure decreases the further you move

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15
Q

Where is pressure greatest in CVS

A

Aorta

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16
Q

Where is pressure lowest

A

Vena Cava

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17
Q

Why does pressure decrease over distance?

A

Resistance

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18
Q

What provides resistance in CVS?

A

“things” in the blood, running into these things, walls of vessels, diameter of vessels

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19
Q

Important relationships of behavior of fluids and gas in CVS

A

Pressure, flow, and resistance

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20
Q

Pressure

A

The force exerted by the fluid or gas on its container
Units: mmHg

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21
Q

2 components of pressure

A

Dynamic and lateral

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22
Q

Dynamic pressure

A

Flowing components that is kinetic energy

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23
Q

Lateral pressure

A

Represents potential energy exerted on the walls of the system (still tech. KE)

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24
Q

Hydrostatic Pressure

A

Energy that is exerted on the walls of blood vessels (lateral movement/pressure)
Use Hydraulic instead because it is not “static”

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25
Q

Friction in CVS

A

The farther the fluid has to flow, it will lose energy due to friction
Sources: blood vessel walls, cells within blood rubbing against each other

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26
Q

What creates pressure in the CVS

A

The heart
As it contracts it creates the driving pressure

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27
Q

Flow depends on…

A

Pressure gradient
Only flows if ∆P is positive
Flow is directly proportional to ∆P
aka higher gradient = higher flow
does NOT depend on absolute pressure

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28
Q

Resistance (R)

A

Forces which reduce the flow of blood
Flow ∝ 1/∆R

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29
Q

Parameters that determine resistance

A

radius of vessel (r)
length of vessel (L)
Viscosity, thickness of blood (fancy n)

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30
Q

Poiseuille’s Law

A

R = Ln/r^4
Resistance increases as length of vessel and/or viscosity increases
Resistance decreases as radius increases

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31
Q

Why is radius of vessel considered the most important factor in providing flow resistance

A

Length of vessels is constant
Viscosity can change but it takes time
So, changing radius is the most common change that will effect resistance
So, really R = 1/r^4

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32
Q

Vasoconstriction

A

decrease in diameter

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33
Q

Vasodilation

A

Increase in diameter

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34
Q

Larger radius implies

A

Less resistance

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35
Q

Flow equation

A

Flow ∝∆P/R

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36
Q

Flow Rate

A

Volume of blood over time (L/min)
It’s how much is going through
Flow higher in large blood vessel

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37
Q

Velocity of flow

A

the speed at which blood flows
Velocity higher in small blood vessel

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38
Q

General heart anatomy

A

~ size of fist
inverted cone with apex (tip) pointed down
Encased in pericardium
4 chambers- R&L atria, R&L Ventricles

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39
Q

Pericardium

A

tough membranous sac with clear pericardial fluid (lubrication to prevent rubbing/friction)

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40
Q

Pericarditis

A

Inflammation of pericardium, increases rubbing

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41
Q

Myocardium

A

composes 99% of heart
Covered by thin epithelial and connective tissue layer

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42
Q

2 Largest veins

A

Superior and inferior vena cava

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43
Q

General flow of blood in heart

A

Through Vena cave to RA
Through right AV valve (tricuspid) to RV
Through pulmonary semilunar valve to lungs
Into LA via pulmonary veins
Through left AV valve (bicuspid) to LV
Through aortic semilunar valve out aorta

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44
Q

Atria

A

Receive blood from vena cava or pulmonary veins; smaller chambers, thinner walls

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45
Q

Ventricles

A

Pump/eject blood into the aorta or pulmonary artery; larger chambers, thick walled
LV larger than right because pressure in aorta is very high and must be overcome by LV to pump blood through it

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46
Q

Common aortic (systolic) pressure

A

120 mmHg

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47
Q

Purpose of valves

A

Prevent backward flow of blood

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48
Q

Atrioventricular valves (AV)

A

B/w atria and ventricles
Tricuspid- RA:RV
Bicuspid (mitral)- LA:LV

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49
Q

Semilunar valves

A

B/w ventricles and their arteries
Aortic- LV:Aorta
Pulmonary- RV:pulmonary trunk

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50
Q

Prolapse

A

Regurgitation of blood b/c valve in wrong place

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51
Q

Stenosis

A

valves don’t open fully (less blood flow)

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52
Q

Incompetent valve

A

valves don’t close (reduces pressure)

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53
Q

Artesia

A

Valves don’t form properly

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54
Q

Chordae tendinae

A

Collagenous tendons that connect AV valves to cardiac muscle

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55
Q

Papillary muscles

A

Extensions of ventricular muscle
Stabilize chordae tendinae, DONT actively open/close valves (pressure does that)

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56
Q

How AV and semilunar valves open/close together

A

Ventricular contraction pushes blood against: AV valves causing them to close and chords prevent prolapse and semilunar valves causing them to open and blood exits ventricle

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57
Q

Coronary circulation

A

Provides blood to heart, different anatomically in everyone
Cardiac muscle uses 70-80% of O2 delivered to it, twice as much as other tissue because of high metabolic demand

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58
Q

Widowmaker

A

Anterior interventricular branch of LCA (LAD)
B/c controls bloodflow to so much myocardium

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59
Q

Primary cardiac muscle cell

A

Contractile cells (myocardium)
Smaller, branched, single nucleated
Adjacent cells joined by intercalated disks
Rely Less on extracellular calcium entry and more on intracellular stores
1/3 cell volume = mitochondria b/c of metabolic demand

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60
Q

Intercalated disks

A

Join adjacent cells
made of desmosomes (cell-cell junction) and gap junction (control ion/molecule movement)

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61
Q

Pacemaker cells (autorythmic)

A

remaining 1%, set the HR (HR can be altered by autonomic nervous system and hormones)
generate action potentials on their own
Concentrated in Sinoatrial node and AV node and bundle branches

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62
Q

HR #s to know: Resting, No Autonomic NS, AV node only, branches only

A

Resting 60-75
No Autonomic 90-95
AV node only 50-60
Branches only 30-45
Default HR is fastest pacemake (SA)

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63
Q

EC-Coupling of contractile cell

A
  1. Action potential enters from adjacent cell, flows down T-Tubule
  2. Voltage gated Ca channel opens, Ca enters cell
  3. Ca induces Ca release from SR via RyR
  4. Release causes Ca spark
  5. Summed sparks create Ca signal
  6. Contraction of sarcomere like skeletal from here
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64
Q

Differences in Contractile cell vs skeletal EC- Coupling

A

No neuromuscular junction
Intracellular Ca more important in cardiac
Ca channel not attached to RyR in cardiac
Relaxation in cardiac also includes Na-Ca exchanger (NCX)

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65
Q

Similarities and differences between Myocardial contractile cell Action potential and skeletal muscle cell

A

Similarities: Na+ entry and K+ exit
Differences: Repolarization is delayed (plateau), resting membrane potential is -90mV instead of -70mV
AP of contractile cell is much longer (~20x)

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66
Q

Myocardial contractile cell AP

A
  1. voltage gated Na+ channels open (voltage comes via gap junctions)
  2. Na+ channels close at peak (+20mV)
  3. Ca channels open, Ca enters cell and keeps mp high, fast K channels close
  4. Ca channels close and slow K channels open, mp decreases
  5. Resting potential reached, no overshoot and hyperpolarization
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67
Q

Ion channels in myocardial contractile cell vs. neuron/skeletal muscle

A

Same Na channels
Dif K channels
Add Ca channels

68
Q

Why do contractile cells have plateau

A

Gives time for blood to fill the chambers while the heart is relaxed

69
Q

Refractory periods of skeletal cell vs. contractile

A

Skeletal refractory periods are very short and can occur multiple times very quickly. They can be summed to reach max tension
Contractile cells have long refractory periods so a second AP can’t be fired until heart is relaxed and filled. NO summation

70
Q

Why use 220 to calculate max HR

A

It is about the time it takes for one refractory period which means that is the fastest the heart can contract

71
Q

why are Autorhythmic cells the pacemakers

A

Unstable membrane potential provide pacemaker ability
Have Pacemaker potential not resting membrane potential

72
Q

If channels (funny channels)

A

Permeable to both Na and K to create current
more NA going in than K out
Slow depolarization (like drip faucet); speed variable
Close once threshold is released

73
Q

Ions responsible for rising and falling face of autorhythmic AP

A

Ca entry is responsible for rising (instead of Na)
K exit is still responsible for falling

74
Q

General AP of Autorhythmic cell

A

Start around -60 mV (approx bc unstable0
1. Slow drip via If channels until threshold (-40 mV instead of -55mv) is reached
2. Ca enters via voltage gated channels, If are closed
3. Ca channels close, K channels open
4. Once return to -60mV K+ channels close and funny open again

75
Q

Why no hyperpolarization in autorhythmic cells?

A

The funny channels open back up again at -60mV preventing it from happening

76
Q

Can you recreate table 14.3 (slide 44)

A

Go do it!

77
Q

Sinoatrial Node (SA)

A

main pacemaker of heart; connected to AV node via internodal pathways

78
Q

How does electrical signal spread through heart

A

SA node –> AV node;
Purkinje fibers, AV bundle, bundle branches
Contraction wave follows electrical signal wave

79
Q

Order of depolarization/electrical conduction

A
  1. SA node depolarizes
  2. Electrical activity goes rapidly to AV node via internodal pathways
  3. Depolar spreads more slowly over atria, conduction slows through AV node
  4. Deplar moves rapidly through ventricular conducitng system to apex
  5. Depolar waves spreads upward from apex
80
Q

Direction of contraction for atria and ventricles

A

Atria contract down
Ventricles contract upward to push blood out aorta/pulmonary vein

81
Q

AV node delay

A

Atria must complete contraction before ventricles begin, so conduction is slightly slower

82
Q

Bundle branch block

A

Ventricle contraction is not simultaneous

83
Q

1st, 2nd, and 3rd degree heart block

A

Signals don’t reach AV node correctly

84
Q

Long-QT syndrome

A

Ventricular contraction and relaxation are delayed

85
Q

If default HR is fastest (SA 90 bpm) why is resting HR 60-70 bpm

A

Autonomic nervous system; Parasympathetic

86
Q

Basics of Electrocardiogram (ECG/EKG)

A

Electrical activity of heart follows a pattern; SUMMED electrical activity of ALL heart cells; basic requires 3 leads (both arms, left leg)

87
Q

Interpretation of EKG depends on

A

Direction electrical wave travels (atrial/vent)
Type of electrical wave (dep/rep)
Whether the lead is positive or negative

88
Q

What charge do depolarizing and repolarizing waves have

A

Depolarizing: Negative
Repolarizing: Positive

89
Q

2 ways to get positive deflection

A

Depolarizing moving TOWARDS positive electrode
Repolarizing moving AWAY from positive electrode

90
Q

3 major components of ECG

A

Waves, segments, intervals

91
Q

Waves

A

Part of ECG trace that goes above/below baseline

92
Q

Segments

A

Sections of baseline between waves

93
Q

Intervals

A

Combinations of waves and segments

94
Q

P -Wave

A

Atrial depolarization

95
Q

QRS complex

A

Ventricular depolarization; hides atrial repoalrization

96
Q

T wave

A

Ventricular repolarization

97
Q

Can u read an EKG?

A

Go do it. slide 55

98
Q

PR Segment

A

Conduction through AV node and AV bundle

99
Q

Diastole

A

Cardiac muscle relaxing; chambers are filling with blood

100
Q

Systole

A

Cardiac muscle is contracting; chambers are ejecting blood

101
Q

Time heart spends in systole vs diastole

A

2/3 time in diastole

102
Q

Late diastole

A

Both sets of chambers are relaxed and ventricles fill passively, pressure higher in atria, AV valves open

103
Q

Atrial Systole

A

Atrial contraction forces a small amount of additional blood into ventricles (complete ventricle filling); quick

104
Q

Heart sound 1

A

After Atrial systole; closing of AV valves because blood pushes back on them

105
Q

Isovolumic ventricular contraction

A

1st phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. Max ventricular blood volume (EDV)
All 4 valves closed

106
Q

Ventricular ejection

A

As ventricular pressure rises and exceeds pressure in the arteries, semilunar valves open and blood is ejected

107
Q

Heart sound 2

A

Dup, Closure of semilunar valves, end of ventricular systole

108
Q

Isovolumic Ventricular relaxation

A

As ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valves and snaps them closed. Minimum blood volume in ventricles (ESV)
All 4 valves shut

109
Q

Pressure Volume loops

A

WORK THROUGH DIAGRAM slide 62

110
Q

Stroke volume

A

EDV - ESV = SV
The amount of blood pumped out by one ventricle during contraction
Not all blood ejected for safety margin
More forceful contraction = more blood ejected

111
Q

Ejection fraction

A

Another way to look at stroke volume;
Percentage of EDV ejected (ESV/EDV)
Normal heart health is 50-70%

112
Q

Cardiac output

A

The volume of blood pumped by one ventricle in a given period of time (L/min)
Measures heart performance and indicator of total blood flow through body
CO = HR * SV
Under autonomic and endocrine control
Typical is about 5 L/min

113
Q

Wiggers Diagram

A

Go through it. lol yikes

114
Q

Sympathetic activity on heart

A

Increase HR (faster depolarization)
Catecholamines increase ion flow of If (Na) and Ca channels
Bind B1-arenergic receptors on autorhythmic cells, increase cAMP
See diagram slide 70

115
Q

Parasympathetic activity on heart

A

Decrease HR
Acetylcholine release binds muscarinic cholinergic receptors
Increase K permeability but decrease Ca permeabaility (doesn’t mess with Na)
Delay depolarization in autorhythmic cells
See diagram slide 70

116
Q

Tonic control of HR

A

Balance, not like a light switch, not either/or
Parasymp dominates at rest
Symp dominates during exercise/stress

117
Q

Preload

A

How much blood fills the ventricle before contraction
Dictated by venous return (blood entering RA); diastolic
Increase preload, increase SV

118
Q

What dictates venous return

A

Skeletal muscle pump
Respiratory pump- thorax movement
Sympathetic constriction of veins
All increases preload

119
Q

Afterload

A

Mean pressure in aorta
The higher mean arterial pressure the harder LV has to work to eject blood
Increase afterload–> decrease SV
Leading cause of heart failure

120
Q

Contractility

A

intrinsic ability of cardiac muscle fiber to contract at any given length
Increase contractility –> increase contraction force (more Ca entry)
Force is Ca dependent

121
Q

Inotropic agents

A

increase or decrease force of contraction (more/less SV)
Catecholamines increase contractility
Other chemicals decrease

122
Q

Heart length-tension relationship

A

Increase length –> increase filling –> increase SV
Only to a point

123
Q

Frank-Starling Law

A

EDV and SV are proportional
Within limits (pericardium sets to prevent too much stretch) heart pumps all blood that enters it
Plateau on graph

124
Q

Cardio calcs + output

A

Go through slide 77!!! and calcs on blackboard/pic

125
Q

General blood vessels composed of

A

Smooth muscle
Connective tissue (elastic and fibrous)
Endotherlial cells (endothelium)

126
Q

One features all blood vessels share?

A

Endothelium

127
Q

Composition of artery

A

Endothelium, elastic tissue, smooth muscle, fibrous tissue

128
Q

Composition of arteriole

A

Endothelium, smooth muscle

129
Q

Composition of Capillary

A

Endothelium

130
Q

Composition of venule

A

Endothelium and fibrous tissue

131
Q

Composition of vein

A

Endothelium, smooth muscle, elastic tissue, fibrous tissue

132
Q

Smooth muscle on blood vessels

A

Controls vasoconstriction and dilation; tonic constriction
Ca-dependent

133
Q

Small vs. large arteries

A

thick and elastic, difficult to stretch, smaller arteries are more muscular

134
Q

Arterioles

A

Major site of resistance
Diameter changes due to smooth muscle

135
Q

Metarterioles

A

bypass capillary beds which reduces flow to tissue

136
Q

Capillaries

A

Regulate exchange, smallest of all vessels
Lack SM and elastic/fibrous tissue
Flat shape helps exchange
Permeability varies by need

137
Q

Venules

A

Similar to capillary
convergent in appearance
SM appears in large ones

138
Q

Veins

A

Thin, large vessels with one way valves
Skeletal muscle pump and respiratory pump aid flow

139
Q

Skeletal muscle pump

A

Aids blood flow in veins
When muscle contracts it compresses the veins and forces blood toward the heart

140
Q

What creates blood pressure

A

Driving pressure: L. vent ejects blood to aorta, aorta expands to accommodate CO, elastic recoil propels blood forward
Obeys fluid flow (pressure gradient)
Arterial pressure is pulsatile (elastic recoil)
Venous pressure is steady

141
Q

Diastolic pressure

A

Aortic pressure during ventricular diastole
Healthy 60-80

142
Q

Systolic pressure

A

Aortic pressure during ventricular systole
Healthy 100-120

143
Q

Pulse pressure

A

PP = systolic - diastolic

144
Q

Mean arterial pressure calculation

A

MAP = diastolic + (1/3)(PP)
MAP = CO * Rarterioles
with CO = HR*SV

145
Q

Venous pressure

A

Approaches 0 in the Vena cava

146
Q

Pulmonary pressure

A

Exists, we will cover later

147
Q

Mean arterial pressure

A

Closer to diastolic pressure because it is longer
Measured with sphygmomanometer

148
Q

Low MAP

A

tissues receive less gases and nutrients

149
Q

High MAP

A

Blood vessel rupture
Causes heart to pump harder (high afterload)
Blood vessels get thicker and stiffer which increases resistance
Capillary damage

150
Q

Mechanisms that alter arteriole resistance

A

Local Control- metabolism, paracrines, auto regulation
Sympathetic reflexes- restrict flow to organs, determine blood distribution
Hormones- regulate salt/water excretion, regulate autonomic reflex control

151
Q

Chemicals that mediate vasoconstriction

A

Norepi, vasopressin, Angiotensin II (most prominent)

152
Q

Chemicals that mediate vasodialation

A

Epi, Nitric oxide (most potent)

153
Q

Myogenic autoregulation

A

Local control of flow
Form of self regulation
Increase in BP –> Increase flow –> Increase SM stretch, vessel then constricts on its own to maintain balance
Strong in brain and kidneys because they need steady, constant blood supply

154
Q

Metabolism as Local flow control

A

Low O2 and high CO2 at arteriole dilates arterioles
Increased flow provides O2 and removes CO2
Active hyperemia

155
Q

Active Hyperemia

A

Increased blood flow in response to increased metabolism

156
Q

Occlusion of BV (local control)

A

Blockage leads to waste accumulation and O2 falls
Endothelial cells produce Nitric oxide (dialator)
When flow resumes, significant vasodilation occurs to clear out waste

157
Q

Reactive hyperemia

A

Vasodilation in response to low perfusion
Similar to active hyperemia but the trigger is different

158
Q

How is the trigger different between reactive and active hyperemia

A

In active an increase in metabolism triggers dilation
In reactive the dilation follows a period of decreased blood flow

159
Q

Sympathetic control of vascular smooth muscle

A

Most arterioles innervated by sympathetic neurons
Norepi bind alpha receptors which causes CONSTRICTION
Dilation achieved by decrease in norepi release
EXCEPTION: arterioles of heart, liver, and skeletal muscle respond to Epi
Epi causes DILATION by binding to B2 (don’t want to constrict these arteries)

160
Q

Brief receptor effect summary

A

B1 on heart –> increase HR, and Ca entry
B2 on BV –> Vasodilation
alpha1 on BV –> vasoconstriction

161
Q

Why is there no parasympathetic dilation if sympathetic mostly constricts arterioles?

A

It would create too quick a drop in BP if parasymp could immediately dilate after constriction by symp.

162
Q

Blood distribution

A

Unequal in body, changes with movement/position
More important organs get more blood per mass unit even if they get less overall quantity of blood

163
Q

Resistance determines path of flow

A

Blood wants to take path of least resistance, so if there is some form of resistance it will deviate itself to go somewhere else

164
Q

What blood flow is almost constant?

A

Cerebral and renal
Stays constant even in stress/exercise because strong myogenic autoreg

165
Q

Coronary flow regulation

A

Exception
Depends on heart activity level
Myocardium release adenosine which causes coronary dilation
*not myogenic autoreg.

A&P lecture 2 (4 decks)

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